Abstract: Objective 　To investigate the effects of moderate aerobic exercise and high intensity intermittent exercise on myocardial mitophagy in mice with nonalcoholic fatty liver disease and its possible mechanism. Methods 　Forty 3-week-old male C57BL/6J mice were randomly divided into a normal feeding group (Chow group, n=10) and high fat-fed group (HFD group, n=30). At week 18, mice in the HFD group with a body weight exceeding 20%~30% of the ordinary diet group were considered obese mice (n=26). Two mice were randomly selected for liver oil red O staining to confirm successful establishment of the NAFLD mouse model. Sixteen NAFLD mice were randomly selected and divided into a moderate intensity aerobic exercise group (MICT group) and high intensity intermittent aerobic exercise group (HIIT group) with eight mice in each group. The two groups were subjected to exercise training for 8 weeks, and samples were weighed after treatment. Masson staining was used to observe myocardial fibrosis. The ultrastructure of myocardial cells was observed by transmission electron microscopy. Mitophagy and mitochondrial biogenesis were assessed by Western blot. Results 　Compared with the Control group, the body weight and heart index in the Model group were significantly increased and decreased, respectively. Compared with the Model group, the body weight of MICT and HIIT groups was increased significantly, and the heart index of the MICT group was increased. Masson staining showed that, compared with the Control group, collagen fiber content in the myocardium in the Model group was significantly increased, and the myocardial fibers were disorganized and broken in electron microscopy. The myocardial morphology was disorganized, mitochondria were swollen, cristae were broken and blurred, and lipid droplets were observed. Compared with the Model group, the myocardial collagen fiber content in MICT and HIIT groups was significantly reduced, the myocardial fiber arrangement had slightly recovered in transmission electron microscopy, the z-line was clearly visible, the degree of mitochondrial degeneration was slightly improved, and lipid droplets were slightly reduced. The improvement in the cardiac tissue structure in the MICT group was better than that in the HIIT group. Western blot showed that, compared with the Control group, PINK1 and Beclin1 expression levels in myocardial tissue of the Model group underwent no significant changes, while Parkin, LAMP1, and PGC-1α expression was significantly decreased (P<0. 01). p62 protein expression and the LC3-Ⅱ/ LC3-Ⅰ ratio were significantly increased (P<0. 05, P<0. 01). Compared with the Model group, PINK1 and Beclin1 expression levels in MICT and HIIT groups were not significantly changed, while PGC-1α expression was upregulated, and Parkin and LAMP1 expression in the MICT group was significantly increased (P<0. 05). p62 protein expression and the LC3-Ⅱ/ LC3-Ⅰ ratio were significantly decreased (P<0. 05, P<0. 01), Parkin and LAMP1 expression levels were upregulated, and the LC3-Ⅱ/ LC3-Ⅰ ratio and p62 protein expression were significantly decreased in the HIIT group (P<0. 05, P<0. 01). Conclusions 　Different forms of aerobic exercise effectively ameliorate myocardial structural and functional injury in NAFLD mice, which may be mediated through stimulating autophagy flux of mitochondria in cardiomyocytes, activating autophagy, and restoring the normal autophagy function of cells to ameliorate myocardial cell damage, and moderate continuous aerobic exercise has a better improving effect.

Abstract: Objective　To study the pathogenesis of hyperuricemia combined with nonalcoholic fatty liver disease (HUA-NAFLD) based on the PI3K/ Akt/ NF-κB signaling pathway. Methods 　Sixty-four SD rats were randomly divided into blank, HUA, NAFLD and HUA-NAFLD groups with 16 rats in each group. Samples were collected at weeks 8 and 12. Serum biochemical indexes were measured. Pathological changes and lipid deposition in liver tissue were observed by hematoxylin-eosin staining and oil red O staining. Relevant proteins in PI3K/ Akt and NF-κB signaling pathways in liver tissues were measured by Western blot. Results 　Compared with the other three groups, the liver index of rats in the HUANAFLD group was increased significantly (P<0. 05) with a large number of fat vacuoles in hepatocytes, s blurred structure of the hepatic cord, and more severe liver histopathology. Compared with the blank group, UA and LDL levels in the HUA group were increased, HDL levels in the NAFLD group were decreased, UA, TC, TG and LDL levels in the HUA-NAFLD group were increased, and HDL levels were decreased (P<0. 05). Compared with the HUA-NAFLD group, TC, TG, and LDL levels were decreased in the HUA group, and UA, TG, and LDL levels in the NAFLD group were decreased (P<0. 05). Compared with the blank group, AKT and p65 phosphorylation levels in the NAFLD group were increased significantly, AKT, PI3K, p65 and IκκB phosphorylation levels in the HUA-NAFLD group were increased significantly. Compared with the HUA-NAFLD group, AKT and p65 phosphorylation levels in the HUA-NAFLD group were decreased significantly (P<0. 05). The IκκB phosphorylation level was decreased significantly in the HUA group. Compared with the HUA group, the p65 phosphorylation level in the NAFLD group was significantly increased (P< 0. 05). Conclusions Compared with the single disease group, the HUA-NAFLD group had more abnormal biochemical indexes and more severe liver lesions. The PI3K/ Akt/ NF-κB signaling pathway might play a major role in the pathogenesis of HUA, NAFLD and HUA-NAFLD.

Abstract: Objective 　To explore the molecular mechanism of ethyl acetate extract of Liujunzi Decoction (EAELD) on energy metabolism in esophageal cancer EC9706 cells in conditioned medium from cancer-associated fibroblasts (CAFs). Methods 　Methyl thiazol tetrazolium assays were used to assess the effect of EAELD on EC9706 cell proliferation. The effects of EAELD on lactate and glucose in the culture supernatant of EC9706 cells in CAF-conditioned medium were assessed by colorimetry. A seahorse system for energy metabolism analysis was used to assess the effect of EAELD on energy metabolism of EC9706 cells in CAF-conditioned medium. Real-time quantitative PCR (qPCR) and Western blot were used to measure mRNA and protein expression of energy metabolism-related molecules. Results Compared with DMEM, except for the 10 μg/ mL group, EAELD had a significant inhibitory effect on EC9706 cell proliferation (P<0. 05). The 30% inhibitory concentration (IC₃₀) of 25 μg/ mL and half inhibitory concentration (IC₅₀) of 40 μg/ mL were selected as low and high doses for subsequent experiments. In EC9706 cells cultured in CAFM, both low and high dose EAELD groups had significantly reduced non-mitochondrial oxygen consumption, basal respiration, maximum respiration, oxygen consumption of ATP synthesis, spare respiration capacity, basal glycolysis, compensative glycolysis, and glycolysis potential (P<0. 01). Lactate content of EC9706 cells was decreased (P<0. 01), mRNA expression of GLUT1 (P< 0. 05, P< 0. 01) was downregulated, and protein expression of p-PKM2, HK2, PKM2 and MCT1 was downregulated (P<0. 01). The high dose EAELD group had downregulated mitochondrial oxygen consumption and basal respiration. The glycolytic ratio of (P<0. 05) and glucose uptake of EC9706 cells were reduced (P<0. 05) and protein expression of p-PKM2 and GLUT1 was downregulated ( P< 0. 01, P< 0. 05). The low dose group of EAELD had downregulated mRNA expression of MCT1 (P<0. 05). Conclusions 　EAELD interferes with the energy metabolism of EC9706 cells in CAF-conditioned medium, and its mechanism may be related to regulation of HK2, PKM2, GLUT1, MCT1 and MCT4 mRNA and protein expression.

Abstract: Objective　To explore the efficacy and potential mechanism of baicalin in regulating the core clinical symptoms of ADHD by Morris water maze and open field tests. Methods 　Thirty SHRs were randomly divided into five groups: model, methylphenidate hydrochloride (MPH), baicalin, baicalin+tetrabenazine, and MPH+tetrabenazine groups with six rats in each group. Another six WKY rats were used as the normal control group. Rats in the MPH group (1. 5 mg/ kg) and baicalin group (150 mg/ kg) were administered the corresponding drugs (1 mL/100 g) by gavage, and those in normal control and model groups were administered an equal volume of normal saline by gavage. In addition to the corresponding drug gavage, rats in MPH+tetrabenazine and baicalin+tetrabenazine groups were subjected to intraperitoneal injection of tetrabenazine (3 mg/ kg) in accordance with body weight (0. 5 mL/100 g). The course was 4 weeks for all groups. Open field and Morris water maze experiments were conducted at predefined time points to record and analyze the result. Results 　In the open field test, the total distance and average speed of rats in the MPH and baicalin groups were significantly lower than those in the model group (P<0. 05). In the Morris water maze test,the latency of rats in the MPH and baicalin groups was significantly shorter than that of the model group (P<0. 05), and the proportion of movement distance and residence time in the target quadrant and the number of times crossing the platform in the MPH and baicalin groups were significantly higher than those in the model group (P<0. 05), and there is no significant difference between the two grups. The total distance and average speed in the baicalin+tetrabenazine group were significantly lower than those in the model group (P<0. 05) and larger than those in baicalin group in the open field test. The latency in the baicalin+ tetrabenazine grup was significantly shorter than that in the model group (P<0. 05) and was significantly longer than that in baicalin group (P<0. 05) in the Morris water maze test. The movement distance and residence time in the target quadrant in the baicalin+tetrabenazine group were higher than model group and significantly lower than those in the baicalin group (P<0. 05). Conclusions 　Baicalin controls the core symptoms of hyperactivity, impulse, and inattention in the ADHD model, and its curative effect may be related to regulation of dopamine vesicle transport.

Abstract: Objective　To investigate the effect of hypoxia inducer cobalt dichloride (CoCl₂ ) on autophagy of 3T3-L1 adipocytes. Methods 　3T3-L1 adipocytes were cultured and induced to mature adipocytes. CoCl₂ was used as an inducer of hypoxia in vitro. Mature adipocytes were divided into control and CoCl₂ treatment groups with various concentrations and times. In accordance with the result, 150 μmol/ L cobalt dichloride was selected to treat adipocytes for 0, 12, 24 and 48 h. Then, the cells were collected for related tests. MTT assays were used to assess cell survival. Expression of HIF-1α, autophagy-related protein LC3-Ⅱ, Beclin-1 and Glut-1 was analyzed by Western blot. The level of autophagy was measured by immunofluorescence. TNF-α and IL-6 levels in culture supernatants of adipocytes were measured by ELISA. Results 　150 μmol/ L CoCl₂ is the optimal intervention concentration to regulate the autophagy level of 3T3-L1 adipocytes. The levels of autophagic activity increased without reduction in cell viability after 150 μmol/ L CoCl₂ intervention in mature adipocytes for 24 h. The expression protein levels of HIF-1α, LC3-Ⅱ, Beclin-1 and Glut-1 were significantly increased in adipocytes. However, the secretion level of inflammatory factors TNF-α and IL-6 did not increased significantly. The level of autophagic activity and cell viability were decreased at 48 h. The expression protein levels of HIF-1α, LC3-Ⅱ, Beclin-1 and Glut-1 were significantly decreased in adipocytes. However, the increased secretion of inflammatory cytokines TNF-α and IL-6 were observed. Conclusions 　Autophagy was moderately activated in adipocytes by 150 μmol/ L CoCl₂ treatment for 24 hours. Autophagy was activated in a HIF-1α-dependent manner, which plays a role in protecting adipocytes from inflammatory damage and improving insulin resistance.

Abstract: Objective　To investigate the mechanism of allicin in improving human peritoneal mesenchymal cellmesenchymal transformation induced by high glucose. Methods 　Human peritoneal mesothelial cells (HPMCs) were divided into the following groups. Group 1: ①Control group; ②8. 5 mmol/ L D-glucose group (8. 5 mmol/ L DG group); ③17 mmol/ L D-glucose group (17 mmol/ L DG group); ④34 mmol/ L D-glucose group (34 mmol/ L DG group); ⑤68 mmol/ L D-glucose group (68 mmol/ L DG group). Except in the control group, the groups were treated with the corresponding concentrations of D-glucose for 48 h. Group 2: ①Control group; ②34 mmol/ L D-glucose group (HG group); ③34 mmol/ L D-glucose + low dose allicin group (AL-L group); ④34 mmol/ L D-glucose + medium dose allicin group (AL-M group); ⑤34 mmol/ L glucose + high-dose allicin group (AL-H group); ⑥34 mmol/ L D-glucose + JAK2 inhibitor group (JAK2 group). The HG group was treated with 34 mmol/ L D-glucose for 48 h. AL-L, AL-M and AL-H groups were pretreated with 34 mmol/ L D-glucose for 6 h and then treated with 10, 20 and 40 ng/ mL allicin for 48 h, respectively. The JAK2 group was pretreated with 1 μmol/ L AG490 for 6 h and then treated with 34 mmol/ L D-glucose for 48 h. IL-6, TNF-α, and IL-1β contents in HPMC culture supernatants were determined by ELISA. A CCK-8 assay was used to assess cell proliferation and morphology. JAK2, p-JAK2, STAT3, p-STAT3, N-cadherin, E-cadherin, Vimentin, α-SMA, MCP-1, p65 and p-p65 protein expression was detected by Western blot. Results 　Compared with the control group, the relative survival rate of HPMCs in the high glucose induced group was significantly reduced (P<0. 01), cell morphology was abnormal, expression of α-SMA, N-cadherin and Vimentin that promote epithelial-mesenchymal transition was significantly upregulated, and expression of E-cadherin, which inhibits EMT, was significantly downregulated. The JAK2/ STAT3 signaling pathway was activated, leading to EMT ( P< 0. 01). Allicin significantly promoted HPMC proliferation induced by high glucose, reversed the abnormal cell morphology, regulated the expression of EMT-related proteins, and improved epithelial-mesenchymal transition of HPMCs. Compared with the high glucose group, proinflammatory cytokines IL-1β, IL-6 and TNF-α in HPMCs in the allicin treatment group were significantly decreased and expression of proinflammatory proteins p-p50 and MCP1 was significantly downregulated, indicating that allicin improved the inflammation caused by EMT. Conclusions 　Allicin improved EMT and inflammation induced by high glucose by inhibiting the JAK2/ STAT3 signaling pathway to regulate the expression EMT markers, inflammatory signaling proteins, and proinflammatory factors.

Abstract: Objective　To investigate the effect of inhibiting the mitochondrial inner membrane protein OMA1 on rotenone (Rot)-Induced apoptosis in a Parkinson’s disease (PD) cell model. Methods 　SH-SY5Y cells were cultured in vitro, treated with Rot (final concentration of 0. 05, 0. 1, 0. 2, 0. 3 or 0. 4 μmol/ L) for 24 h, and the best Rot concentration (0. 2 μmol/ L) was selected for subsequent experiments. The cells were divided into a control group (without special treatment), PD model group (0. 2 μmol/ L Rot treatment for 24 h), negative control group (control group which was transfected with OMA1 negative sequence), and OMA1 siRNA group (0. 2 μmol/ L Rot treatment for 24 h and transfection with OMA1 siRNA). CCK-8 was used to detect cell survival rate, and an inverted phase-contrast microscope was used to observe cell morphology in each group. Western blot was used to detect changes in the expression of OMA1 and the apoptosis-related proteins Caspase-3, Bax and Bcl-2, and a TUNEL apoptosis kit was used to detect cell apoptosis. Results 　Compared with the control group, the survival rate of SH-SY5Y cells decreased in a concentration-dependent manner with increasing Rot concentration (P<0. 05). Compared with the control group, the PD model group’s expression of OMA1 and the apoptotic protein Caspase-3 and the ratio of Bax/ Bcl-2 were increased (P<0. 01). Compared with in the PD model group, in the OMA1 siRNA group cells, morphological changes gradually restored, apoptotic protein Caspase-3 expression decreased, Bax/ Bcl-2 increased, and TUNEL apoptosis staining suggested reduced apoptosis (P< 0. 01). Conclusions 　Inhibition of the mitochondrial inner membrane protein OMA1 ameliorated the apoptosis induced in the Rottreated PD cell model, and in turn, may have a protective effect on neurons.

Abstract: Objective　To summarize the important points of animal models of osteosarcoma and to provide a reference and suggestions to improve the modeling method and evaluation indexes. Methods 　Using osteosarcoma and animals as the main topics, literature on animal models of osteosarcoma from CNKI, Wanfang Data and PubMed. The species of experimental animals, gender, modeling method, types of cancer cell lines and detection indicators were summarized, and a database was established for statistical analysis. Results 　A total of 284 reports were included. The most selected osteosarcoma model animals were BALB/ c-nu/ nu mice (227 times, 75. 17%), followed by SD rats (20 times, 6. 62%). Subcutaneous cell fluid transplantation in the back (66 times, 21. 85%), subcutaneous cell fluid transplantation in the axils (55 times, 18. 21%), and in situ cell fluid transplantation (51 times, 16. 89%) were used as modeling method . Human MG-63 cells (100 times, 33. 11%) and mouse UMR-106 cells (39 times, 12. 91%) were selected as the cancer cell line. The most analyzed indexes were the tumor tissue apparent index (238 times, 83. 80%), HE staining of tumor tissue ( 129 times, 45. 42%), and Animal epigenetic metrics ( 94 times, 33. 10%), and immunohistochemistry of tumor tissue (89 times, 31. 34%). Conclusions 　At present, osteosarcoma BALB/ c-nu/ nu mice aged 4 to 6 weeks are used as experimental animals, and human MG-63 cell heterotopic transplantation (back and axillary transplantation) is used to establish the animal model, and the detection indexes of osteosarcoma are comprehensively evaluated by animal apparent index, tumor apparent index and tumor histopathology. It is suggested to select serum biochemical index, apparent index of tumor tissue as well, HE staining of tumor tissue and immunohistochemistry of tumor tissue to evaluate the model. However, there is still a lack of animal model preparation and evaluation criteria with high clinical consistency. In this paper, the advantages and disadvantages are summarized through literature mining and data analysis, in order to provide reference for the establishment of a good OS model and better application to OS mechanism research and new drug development.

Abstract: Objective　To explore the mechanism by which long non-coding RNA SNHG16 (lncRNA SNHG16) promotes liver cancer cell resistance to sorafenib by regulating microRNA-570 (miR-570). Methods Real-time fluorescent RT-PCR was used to detect lncRNA SNHG16 and miR-570 expression of human normal liver tissue and liver cancer cells, HepG2 and HepG2-R. HepG2-R cells were transfected to provide the following groups: HepG2-R+pcDNA, HepG2-R+ pcDNA SNHG16, HepG2-R+anti-miR-NC, HepG2-R+anti-miR-570, and HepG2-R+pcDNA group. HepG2-R+SNHG16+ miR-NC and HepG2-R+pcDNA SNHG16+miR-570 groups were used for follow-up tests. miR-NC, miR-570, si-NC, and si-SNHG16 were transfected into HepG2 cells in the same way to give HepG2+miRNC, HepG2+miR-570, HepG2+si-NC, and HepG2+si-SNHG16 groups. MTT assay, flow cytometry and Transwell assay were used to detect cell proliferation, apoptosis, and invasion. Western blot assay was used to detect the changes in expression of CyclinD1, P21, MMP-9, and MMP-2. Results 　Compared with normal liver tissue, the liver cancer tissue showed increased lncRNA SNHG16 and decreased miR-570 expression (P< 0. 05). Compared with the normal cell HepG2-P group, the HepG2-R group had increased lncRNA SNHG16 and IC₅₀ values, and the inhibition rates of miR-570 in HepG2-R cells were decreased at sorafenib concentrations of 1, 2, 4, 8, 16 μmol/ L (P<0. 05). In the HepG2-R+pcDNA SNHG16 overexpression group, lncRNA SNHG16 expression was significantly increased (P<0. 05). Compared with the HepG2-R+pcDNA group, the HepG2-R+pcDNA SNHG16 group’s number of migrated cells and expression of CyclinD1, P21, MMP-9, and MMP-2 were decreased, while the inhibition rate, apoptosis rate, and P21 expression were increased (P<0. 05). Compared with the HepG2-R+anti-miR-NC group, the HepG2-R+anti-miR-570 group’ s miR-570 levels were decreased (P< 0. 05). Compared with the HepG2-R + anti-miR-NC group, the HepG2-R + anti-miR-570 group showed decreased levels of CyclinD1, MMP-9, and MMP-2 and increased inhibition rate, apoptosis rate, and P21 expression (P<0. 05). A dual luciferase reporting experiment showed that, compared with the miR-NC group, miR-570 reduced WT-SNHG16 luciferase activity (P<0. 05), but there was little effect on the luciferase activity of MT-SNHG16 (P>0. 05). Overexpression of lncRNA SNHG16 decreased the expression of miR-570 in HepG2-R cells (P< 0. 05). Compared with the HepG2-R+ pcDNA SNHG16+ miR-NC group, the HepG2-R + pcDNA SNHG16 + miR-570 group’ s number of migrated cells and expression levels of CyclinD1, MMP-9, and MMP-2 were increased, while the inhibition rate, apoptosis rate, and P21 expression were decreased (P<0. 05). Conclusions 　lncRNA SNHG16 can regulate the drug resistance of HepG2-R liver cancer cells. The mechanism is related to the targeted regulation of miR-570 by lncRNA SNHG16, thus miR-570 provides a new target for the clinical treatment of liver cancer cells.

Abstract: Objective 　To establish an effective and reliable chronic alcoholic brain injury model in mice. Methods 　Forty C57BL/6J mice were randomly assigned to a control group or a model group. Mice in the model group were given free access to 5% (v/ v) alcohol in drinking water and were intragastrically administered 28% (v/ v) alcohol. The gavage dosage increased gradually over the first two weeks (from 0 g/ kg to 6 g/ kg body weight) and remained at 6 g/ kg body weight for the subsequent four weeks. Mice in the control group were provided with normal water and given the same amount of saline via gavage. At the end of the experiment, the cognitive function and motor ability of the mice were evaluated through behavioral tests. Morphological changes in the brain tissue of mice were examined by histopathological staining. Results 　Compared to mice in the control group, mice in the model group showed cognitive impairments and motor dysfunction in the behavioral tests. Pathological examination of brain tissue from the model group mice showed morphological damage and cell necrosis in the hippocampus. Conclusions 　A mouse model of chronic alcoholic brain injury was effectively established in this study, providing a valuable tool for investigating the underlying mechanisms of and potential drug interventions for chronic alcoholic encephalopathy.

Abstract: Objective　To investigate the effect and mechanism of long non-coding RNA (LncRNA) FGD5-AS1 on the proliferation, apoptosis, migration, and invasion of oral squamous cell carcinoma (OSCC) cells. Methods 　FGD5- AS1 expression in OSCC was analyzed using an online database. Tumor and normal tissues of 30 patients with OSCC collected at the Stomatology Department of Tengzhou Central People’s Hospital, and human oral mucosal cell line HOK and OSCC cell lines SCC-9, HSC-4, SCC-25, and CAL-27 cultured in vitro were investigated. qRT-PCR was performed to measure FGD5-AS1 and miR-129-5p expression. CAL-27 cells with the highest FGD5-AS1 expression were divided into Control, si-NC, si-FGD5-AS1, si-FGD5-AS1+NC inhibitor, and si-FGD5-AS1+miR-129-5p inhibitor groups. CCK-8 and colony formation assays were used to assess cell proliferation. Apoptosis was detected by flow cytometry. Cell migration was assessed by wound healing assays. Transwell chambers were used to assess cell invasion. Dual luciferase reporter assays were sued to verify the targeting relationship between FGD5-AS1 and miR-129-5p. Expression of high mobility group protein B1 (HMGB1) was detected by Western blot. An In vivo xenograft tumor model was established and divided into sh- NC, sh-FGD5-AS1, miR-129-5p inhibitor, and sh-FGD5-AS1+miR-129-5p inhibitor groups. The tumor volume and tumor were assessed. qRT-PCR was used to measure FGD5-AS1 and miR-129-5p expression in transplanted tumor tissues. HMGB1 and Ki67 expression was detected by immunohistochemistry. Results 　Database analysis showed that the expression level of FGD5-AS1 in OSCC tumor tissues was 4 times higher than that in normal tissues. FGD5-AS1 expression was associated with a poor grade in OSCC patients. Compared with normal tissues and human oral mucosal cells, FGD5- AS1 expression in tumor tissues and OSCC cell lines was significantly increased, and miR-129-5p expression was significantly decreased ( P< 0. 05). CAL-27 cells with the highest expression level of FGD5-AS1 were selected for transfection experiments. Silencing FGD5-AS1 increased the apoptosis rate, decreased cell viability, the scratch healing rate, and number of invaded cells, enhanced miR-129-5p expression, and downregulated HMGB1 expression (P<0. 05). MiR-129-5p was the target gene of FGD5-AS1. Inhibition of miR-129-5p expression reversed the effects of silencing FGD5- AS1 on OSCC cell proliferation, apoptosis, migration, and invasion. In vivo experiments showed that FGD5-AS1 silencing significantly inhibited tumor growth and expression of HMGB1 and Ki67 (P<0. 05), and inhibition of miR-129-5p result ed in the opposite trend. Inhibition of miR-129-5p reversed the effects of FGD5-AS1 inhibiton on tumor growth and expression of HMGB1 and Ki67 (P<0. 05). Conclusions 　FGD5-AS1 is upregulated in OSCC cells. Interfering with FGD5-AS1 expression inhibit the proliferations, migration, and invasion of OSCC cells and promotes apoptosis by targeting the miR- 129-5p/ HMGB1 axis.

Abstract: Objective　To investigate the influence of hypericin (Hyp) on renal autophagy and the AMPK/ mTOR/ ULK1 pathway in nephrotic syndrome (NS) rats. Methods Thirty-two 6-week-old SD rats were grouped into normal (N), NS, Hyp (60 mg/ kg Hyp), and Hyp+CC (60 mg/ kg Hyp+0. 2 mg/ kg CC AMPK inhibitor) groups, with eight rats per group. The NS model was established by one-time injection of adriamycin (6.5 mg/ kg) through the tail vein, and the success rate of the model was 75. 0%. Rats in the Hyp group were given 60 mg/ kg Hyp intragastric administration; rats in the Hyp+CC group were given 60 mg/ kg Hyp intragastric administration and 0. 2 mg/ kg CC intraperitoneal injection; and rats in the N and NS groups were given the same amount of solvent once a day for 14 days. After administration, an automatic analyzer was applied to detect the levels of 24-h urine total protein (UTP), blood urea nitrogen (BUN), serum creatinine (Scr), and albumin (ALB). HE staining was used to observe the pathological morphology of the kidney tissue. The ultrastructure of the renal tissue was observed by transmission electron microscope. Western blot was applied to detect the expression of autophagy, podocyte, and AMPK/ mTOR/ ULK1 pathway proteins in the kidney. Immunofluorescence staining was applied to visualize the localization of autophagosomes and podocytes. Results 　Compared with the N group, the NS group had increased glomerular volume; atrophied or partially disappeared renal tubules; a thickened basement membrane; and obviously increased UTP, BUN and Scr levels, basement membrane thickness, foot process width, and p-AMPK/ AMPK ratio (P<0. 05), while the levels of ALB, LC3-II/ I, Beclin-1, Atg5, Atg7 and NPHS2; the relative fluorescence intensity of NPHS2 and Beclin-1; and p-AMPK/ AMPK and p-ULK1/ ULK1 ratios were obviously decreased (P<0. 05). Compared with the NS group, the Hyp treatment group had improved glomerular morphology and decreased UTP, BUN, and Scr levels, basement membrane thickness, foot process width, and p-AMPK/ AMPK (P<0. 05) ratio, but there was an increase in the protein levels of ALB, LC3-II/ I, Beclin-1, Atg5, Atg7, NPHS2; relative fluorescence intensity of NPHS2 and Beclin-1; and p-AMPK/ AMPK and p-ULK1/ ULK1 ratios (P<0. 05). Compared with the Hyp group, the Hyp+CC group’ s glomerular volume increased; renal tubules atrophied or partially disappeared; basement membrane thickened; and UTP, BUN, Scr levels, basement membrane thickness, foot process width, and p-AMPK/ AMPK ratio were obviously increased (P<0. 05), whereas the protein levels of ALB, LC3-II/ I, Beclin-1, Atg5, Atg7, and NPHS2; relative fluorescence intensity of NPHS2 and Beclin-1; and p-AMPK/ AMPK and p-ULK1/ ULK1 ratios were obviously decreased (P<0. 05). Conclusions 　Hyp may enhance the autophagic activity of renal cells and attenuate renal pathology, such as podocyte injury, in NS rats by activating the AMPK/ mTOR/ ULK1 pathway.

Abstract:Parkinson’ s disease (PD) is a neurodegenerative disease. Its pathogenesis is currently unknown. Patients may present with motor and non-motor symptoms. To explore the mechanisms underlying these phenotypes, appropriate animal models are needed. Rodent models only partially recapitulate the symptoms of PD. Therefore, relevant preclinical studies are limited. Non-human primate animal models are better able to recapitulate such symptoms. Quantifying motor and non-motor symptoms in non-human primate models of PD is useful to study its pathogenesis and treatment. This review summarizes various approaches to quantifying behavioral paradigms and compares the advantages and disadvantages of the approaches. It also provides a reference for behavioral testing in PD monkey models.

Abstract:Alzheimer’s disease (AD) is an irreversible heterogeneous neurodegenerative disease. AD patients have memory loss and impaired synaptic plasticity. In view of cAMP responsive element-binding protein (CREB), which is intimately associated with synaptic plasticity, this article summarizes the research progress on the structure, signaling pathways, downstream genes, and relative memory regulation. The involvement of CREB in AD development serves as a reference for AD researchers to improve synaptic plasticity.

Abstract:Ischemic stroke is a cerebrovascular disease that leads to high incidences of disability and mortality and can be life-threatening in severe cases, thus, it has a heavy social and economic burden worldwide. The etiology and pathological processes of ischemic stroke are mediated by a variety of molecular processes, some of which are dynamically regulated after transcription. Increasing evidence has shown that micro ( mi)-RNA, as important mediators of posttranscriptional gene silencing, play crucial roles in gene expression and the pathological processes of ischemic stroke. In this review, we discuss the neuroprotective effects of miRNAs in the different mechanisms involved in ischemic stroke. As the promotion or inhibition of miRNA expression through specific drug and non-drug therapies may be beneficial to the recovery of ischemic stroke, the use of miRNA in clinical diagnosis and treatment are also discussed in detail in this paper. This article aims to provide a reference for further clinical and basic research in this field.

Abstract:The liver is the most common organ for tumor spread, and expression of miRNA is crucial for liver metastasis. In this study, research progress of related miRNAs in regulating liver metastases from malignant tumors in the digestive system was collated and analyzed. By searching related literature, this article provides an introduction to the role of miRNAs in liver metastasis of colorectal, gastric, pancreatic, and gallbladder cancers, which helps with the diagnosis, treatment, and research of tumor liver metastasis.

Abstract:The lymphatic system plays an important role in regulating interstitial fluid homeostasis, lipid metabolism, and immune functions. After myocardial infarction, enhanced lymphangiogenesis accelerates clearance of infiltrating immune cells, reduces production of proinflammatory cytokines, reduces edema, inflammation, and fibrosis, and promotes recovery of impaired heart functions. Vascular endothelial growth factor-C (VEGF-C) and its receptor, VEGFR-3, are components of the lymphangiogenesis pathway and play a critical role in maintaining the tissue fluid balance and myocardial functions after cardiac injury. Lymphatic vessels are closely related to the immune system. Various immune cell populations stimulate or inhibit lymphatic remodeling. Macrophages are congenital immune cells distributed widely in organs and tissues, play an important role in various physiological and pathological processes such as organ development, host defense, acute and chronic inflammation, and tissue homeostasis and remodeling. More mechanisms of lymphangiogenesis need to be clarified to provide effective targets for clinical stimulation of lymphangiogenesis to treat heart disease. This article reviews basic pathological changes of the heart and lymphatic vessels after myocardial infarction, the regulatory factors of lymphangiogenesis, and the influence of macrophages on lymphangiogenesis.

Abstract:Monkeypox is an infectious disease caused by monkeypox virus (MPXV) infection. The host of MPXV remains unclear, and rodents and non-human primates are considered to be potential hosts. Monkeypox is rapidly spreading worldwide. However, animal models of monkeypox have not been established in China. MPXV is a pathogen that seriously threatens human health. Its transmission among the population has presented new characteristics. Therefore, this article describes the discovery of MPXV and the early epidemic, different types of infection, and coinfection. Additionally, experimental infection and animal models of monkeypox in rodents and non-human primates are expounded.

Abstract:Alzheimer’ s disease (AD) is an invasive neurodegenerative disease, the cause of which is still unknown. Neuroinflammation is a chronic inflammatory response activated by microglia and astrocytes in the central nervous system that is closely related to the release of many inflammatory factors and the destruction of the blood-brain barrier. Studies have shown that neuroinflammation is the third largest pathological change in AD after β-amyloid deposition and neurofibrillary tangles. In this paper, the information available on microglia, astrocytes and their interactions is summarized. The roles of these cells in neuroinflammation and AD are presented and discussed to provide a theoretical and experimental reference for the pathogenesis, prevention, and treatment of AD.

Abstract:In recent years, hepatitis B virus (HBV)-Infected patients with diffuse large B cell lymphoma (DLBCL) have increased. Its etiology is complex and treatment is difficult. Therefore, it has received extensive research attention. By reviewing and analyzing the studies of domestic and foreign researchers, this article discusses the mechanism of the occurrence and development of DLBCL caused by HBV infection and the clinical prognosis of patients. The findings suggest that, at genomic and transcriptome levels, HBV mainly induces changes in the expression of BCL6, FOXO1, ZFP36L1 and other genes, and activate various regulatory genes through the HBV X protein, thereby inducing clonal proliferation of lymphocytes and eventually forming lymphoma. The prognostic assessment mainly analyzes and compares the patient age of onset, sex, organ involvement, international prognostic index, lactate dehydrogenase level, proliferation index (Ki-67), bcl-2, bcl-6, inflammatory index, and other factors, to propose a theoretical basis for clinical diagnosis and treatment of DLBCL and basic research.