Abstract: Objective Siwu mixture is derived from Siwu decoction, a classical Chinese medicine prescription, which is widely used in a variety of gynecological diseases. However, There are few studies on the therapeutic effect of Siwu mixture on primary dysmenorrhea. This study aims to further explain its therapeutic effect. Methods Sixty healthy animals were divided into four groups: the control group, model group, Siwu mixture group and Tongjingbao granule group. The primary dysmenorrhea mice model was induced by estrogen combined with oxytocin. After 3 days of adaptive feeding, mice were subcutaneously injected with estradiol benzoate 2 mg / kg for 10 days. The normal and the model group received the same dosage of distilled water from the 4th day. The Tongjingbao granule group was given 4 g / kg for 7 days. The Siwu mixture group was given 8 mL/ kg for 7 days. The analgesic effect of Siwu mixture was studied by writhing and the latency of writhing within 30 min after oxytocin injection. The serum contents of malondialdehyde (MDA) and superoxide dismutase (SOD) were determined. ProstaglandinF_2α (PGF_2α ), interleukin-6 ( IL-6) and tumor necrosis factor-α (TNF-α) were measured in tissue homogenates by ELISA method. Uterine pathological sections were prepared to observe glandular hyperplasia and inflammatory cell infiltration, and the expression of cyclooxygenase-2 ( COX-2 ) was detected by immunohistochemistry. Results Compared with result in the control group, the body twisting in the model group increased (P<0. 01) and serum MDA increased (P<0. 01). Uterine tissue PGF_2α , TNF-α and IL-6 increased. In the model group, endometrial glands were dilated and papillary hyperplasia, interstitial edema, inflammatory cell proliferation and infiltration were observed; COX-2 expression was enhanced. The number of writhing events within 30 min in Tongjingbao granule group and Siwu mixture group decreased compared with controls (P<0. 05, P<0.01); the writhing latency in the Siwu mixture group increased (P<0.05) and the level of serum MDA in the positive drug group and Siwu mixture group decreased (P< 0.01). Conclusions Siwu mixture could significantly reduced the 30 min writhing times and prolonged the writhing latency of primary dysmenorrhea mice. The mechanism may be related to reducing the content of serum MDA and PGF_2α , TNF-α and IL-6 in uterine tissue and COX-2 expression are related to the improvement of histopathological changes.

Abstract: Objective To observe the effect of overexpression of lysosome associated membrane protein 2A (LAMP2A) up-regulating chaperone-mediated autophagy (CMA) in the substantia nigra on the locomotor behavior of a Parkinson’s disease (PD) rhesus monkey model. Methods We established a rhesus monkey model of PD. A stereotactic injection device was used to inject Lewy bodies (LBs) extracts from the brain tissues donated by PD patients into the right striatum of seven rhesus monkeys. At the same time, extracts of brain tissue donated by control ( non-PD) patients were injected into the striatum of the left brain. The animals were randomly divided into two groups. The LAMP2A overexpression group (n= 4) was bilaterally injected with an adeno-associated virus vector overexpressing LAMP2A; the control group (n= 3) was injected with a control virus vector in both sides of the substantia nigra. The motor function of monkeys was evaluated by the hill and valley staircase experiment and the pick-up test. The levels of total α-synuclein ( α-syn) and phosphorylated α-syn in the cerebrospinal fluid and serum of experimental monkeys were determined by ELISA. Results In the valley staircase task and the outside board pick up test, the fine motor level of the left upper limb of the control group of rhesus monkeys was lower than that of the right side. There was no significant difference in the fine motor level of the upper limbs on the left and right sides of the rhesus monkeys in the LAMP2A overexpression group. Cerebrospinal fluid and serum total α-syn levels and phosphorylated α-syn levels of the control group increased significantly at 12 months after operation. The levels of phosphorylated α-syn in cerebrospinal fluid and serum phosphorylated α-syn in the LAMP2A overexpression group were lower than those in the control group at the same time after 8 months. Conclusions Overexpression of LAMP2A improved the fine motor ability of experimental monkeys in the rhesus monkey model of PD through up-regulating CMA-mediated α-syn elimination.

Abstract: Objective To evaluate the effect of different levels of doxorubicin-induced cardiotoxicity in mice by examining pathological changes. Methods In total, 36 male C57BL/ 6J mice (8 weeks old, SPF grade) were randomly assigned to the normal saline group ( NS group), 3 mg / kg doxorubicin group, 4 mg / kg doxorubicin group, 5 mg / kg doxorubicin group, 6 mg / kg doxorubicin group and 7 mg / kg doxorubicin group ( 6 mice in each group). Mice received intraperitoneal injection of saline or different concentrations of doxorubicin, 3 days/ times, 10 times in total. We monitored heart weight, body weight, ratio of body weight with heart weight, tibia to heart weight ratio, survival rate and evaluated cardiomyocyte apoptosis and cardiac fibrosis, simultaneously measured the cross-sectional area of heart and single myocyte cross-sectional area size. Results All six mice in each of the 3~ 5 mg / kg groups survived, with a survival rate of 100%. Five mice in the 6 mg / kg group survived, the survival rate was approximately 83. 3%. One mouse in the 7 mg / kg group survived, the survival rate was approximately 16. 7%. The survival rate of mice in the treatment groups decreased and was negatively correlated with doxorubicin concentration. The heart weight, body weight and heart to tibia ratio of mice in the treatment groups decreased in a dose-dependent manner. When the concentration of doxorubicin reached 4 mg / kg, the proportion of cardiomyocyte apoptosis increased, the area of myocardial fibrosis increased, and the cross-sectional area of the whole heart and cardiomyocyte decreased in the model groups compared with the NS group, and these differences were statistically significant (P<0. 05). Conclusions The indexes of cardiac fibrosis, cardiomyocyte apoptosis, atrophy and survival rate of mice worsen with the increase of doxorubicin accumulation in vivo. A concentration of 4 ~ 6 mg / kg doxorubicin is appropriate to build the model of chronic cardiotoxicity in mice, if doxorubicin exceeds this dose, the death rate of mice will be high, which is not conducive to the later experiment.

Abstract: Objective To investigate the effect of fentanyl combined with propofol on cardiac autophagy and cardiac ischemia reperfusion injury (I/ R) in rats. Methods Thirty healthy male SPF SD rats were randomly divided into five groups: the sham group, model group, fentanyl group, propofol group and fentanyl+propofol group. The I/ R model was established for all groups except the sham group. The fentanyl group, propofol group and fentanyl+propofol treatment group were pretreated with 20 μg / kg fentanyl, 50 mg / kg propofol and 20 μg / kg fentanyl combined with 50 mg / kg propofol, respectively. After 30 min, the rats were sacrificed and heart tissue was collected for analyses. HE and TUNEL staining were used to observe the pathological injury of rat heart tissue, TTC staining was used to observe the area of myocardial infarction and electron microscopy was used to observe mitochondrial structure. Western blot was used to detect the expression of autophagy-related proteins Beclin1, ATG5 and L3B. Results Myocardial pathological changes were observed in the model group but not the sham group; in addition, the percentage of cardiac cell apoptosis and infarct area were increased, mitochondrial swelling in myocardial cells was observed and the expression of autophagy-related proteins Beclin1, ATG5 and L3B-II were increased. Treatment of 20 μg / kg fentanyl, 50 mg / kg propofol and 20 μg / kg fentanyl combined with 50 mg / kg propofol pretreatment significantly reduced myocardial pathological injury, cardiac apoptosis and percentage of infarct area in I/ R rats. The treatments alleviated mitochondrial swelling in myocardial cells and decreased the expression of autophagy-related proteins Beclin1, ATG5 and L3B-II. Pretreatment of 20 μg / kg fentanyl combined with 50 mg / kg propofol showed the best performance among the three treatments; there was no significant difference between fentanyl and propofol. Conclusions Both fentanyl and propofol inhibit autophagy, alleviate mitochondrial swelling and reduce myocardial I/ R injury. There was not a significantly different effect between 20 μg / kg fentanyl and 50 mg / kg propofol in the treatment of myocardial I/ R injury. In addition, the combination of fentanyl and propofol had a synergistic effect on myocardial I/ R injury.

Abstract: Objective The purpose of this study was to investigate the effect of total flavones of Desmodium triflorum, calycosin and formononetin from D. triflorum on mice with dextran sodium sulfate ( DSS)-induced ulcerative colitis (UC) and analyze the effects on intestinal flora. Methods Thirty C57BL/ 6 mice were treated with 3% DSS to establish the UC model and divided into the normal group, model group, total flavones of Desmodium triflorum group (500 mg / kg), calycosin group (100 mg / kg) and formononetin group (100 mg / kg). Body weight changes, disease activity index (DAI), colon histopathology score and IL-1β and IL-6 cytokine expression levels in the serum of the mice were determined, and changes of intestinal flora in mice were detected by high-throughput sequencing. Results Administration of total flavones of D. triflorum, calycosin and formononetin from D. triflorum effectively alleviated colonic inflammatory symptoms and reduced the expression of inflammatory factors in UC mice, Resulting in a good therapeutic effect. Treatment with total flavones of D. triflorum, calycosin and formononetin from D. triflorum significantly increased the diversity of intestinal microflora. The proportion of Helicobacteraceae was decreased and those of Muribaculaceae and Lachnospiraceae were increased at the family level. The proportion of Bacteroides was decreased and that of Lactobacillus was increased at the genus level. Regarding the species level, the proportions of Bacteroides and Escherichia coli were decreased. Conclusions Total flavones of D. triflorum, calycosin and formononetin from D. triflorum improve the changes of physical signs and inflammatory factors of UC mice and had a good recovery effect on intestinal flora.

Abstract: Objective This study aimed to establish a reliable animal model of Alzheimer’ s disease (AD) with phlegm and stagnation to provide a corresponding animal model for the prevention and treatment of AD by Chinese medicine and to provide a reference on animal modelling method ology for the establishment of animal models combining disease and TCM evidence. Methods APP / PS1 2×Tg mice were used as AD model animals. The pathological state of “ stasis” was simulated by ice water bath and the pathological state of “ phlegm” was simulated by high-fat diet feeding. The two were combined to simulate the pathological state of “ phlegm and stasis interconnection”. The mice in different groups were treated differently: the AD-phlegm group was given a high-fat diet, the AD-stasis group was given an ice-water bath, the AD-phlegm-stasis group was given both a high-fat diet and an ice-water bath, and the AD-disease model group was left untreated. Non-transgenic C57BL/ 6J mice with the same genetic background were the control group. The differences in AD- like behavioral changes,objective changes in tongue image, blood rheology and lipid alterations and relevant protein content in hippocampal tissue were examined at 14 days after modeling. Results After 14 days of modeling, the AD-like behavioral changes and relevant protein content of mice in the AD groups were significantly changed compared with those in the control group. The tongue color was dark red in the AD-disease model group compared with result in the AD-model group; the hemorheology index of the AD-stasis group and the blood lipid index of the AD-phlegm group were increased. The related indexes of AD-phlegm-stasis interconnection group were significantly increased. Conclusions The combination of ice-water bath and high-fat diet to treat APP / PS1 mice for 14 days successfully established the combined animal model of AD-phlegm-stasis syndrome. This method has a high modeling rate, fits well with clinical symptoms and may represent a useful experimental animal system for subsequent studies.

Abstract: Objective To explore the differentiation of HepG2 cells induced by mouse embryonic hepatocytes at day 13. 5 of gestation through the inhibition of β-Catenin. Methods The distribution of hepatocyte marker molecule- albumin (ALB) was detected by immunofluorescence to identify the hepatocytes of mouse embryo on day 13. 5. After HepG2 cells were co-cultured with embryonic hepatocytes at day 13. 5 of gestation for 24 h and 48 h, the mRNA expressions of AFP (biomarker of hepatocellular carcinoma), HNF-4α (controller of hepatocyte differentiation), CYP1B1 (biomarker of mature hepatocytes) and ADH1C ( another biomarker of mature hepatocytes) were measured by reverse transcriptional quantitative polymerase chain reaction (RT-qPCR). After HepG2 cells were co-cultured with day 13. 5 of gestation embryonic hepatocytes for 48 h, the morphology was observed; AFP, HNF-4α and β-catenin expressions were measured by Western blot and β-Catenin distribution was determined by immunofluorescence. Following treatment with the β-catenin inhibitor, morphology was observed and AFP content was measured. Results Most cells were ALB-positive. The relative mRNA expression of AFP decreased significantly after 24 h and 48 h co-culture, and HNF-4α, CYP1B1 and ADH1C increased significantly at 24 h and 48 h co-culture compared with the levels in the controls. The proliferation of HepG2 cells was suppressed and cell morphology tended to be hexagonal like normal hepatocytes; AFP protein content decreased and HNF-4α protein content increased after co-culture with embryonic hepatocytes at day 13. 5 of gestation for 48 h. Compared with the levels in the control, β-Catenin protein content decreased in the co-culture group and β-catenin was markedly attenuated in the co-cultured HepG2 cells in immunofluorescence result. Compared with the effects in the control group, β- catenin inhibitor treatment caused notable morphological changes of HepG2 cells and induced more dramatic morphological changes of HepG2 cells; furthermore, it reduced AFP protein content. Conclusions HepG2 cells may be induced to undergo differentiation by embryonic hepatocytes at day 13. 5 of gestation mainly through the suppression of β-catenin.

Abstract: Objective To establish a HepG2 cell line with downregulated heterogeneous nuclear ribonucleoprotein K (HNRNPK) mediated by lentivirus and study the effects of HNRNPK downregulation on cell proliferation and migration. Methods HepG2 cells were infected with packaged lentivirus, and positive cells were selected to obtain stable transgenic cell lines. Then detected expression efficiency of HNRNPK. The effect of HNRNPK downregulation on cell proliferation was detected using cell counting CCK-8 and colony formation assays. The effect of HNRNPK downregulation on cell migration was detected using the wound healing and Transwell assays. Results The HepG2 cell line with downregulated HNRNPK mediated by lentivirus infection was successfully constructed. HNRNPK-downregulation inhibited the proliferation and migration of HepG2 liver cells. Conclusions HNRNPK-downregulation inhibits the proliferation and migration of HepG2 liver cells in vitro.

Abstract: Objective Cardiac hypertrophy (CH) is classified into physiologic and pathological types; it can be induced under chronic stress and is an independent risk factor for heart failure. Previous reports have suggested that drug delivery routes and dosage of isoprenaline ( ISO) vary widely. The pathological characteristic of CH animal models varies induced by ISO treatment. Methods We established a rat CH model by subcutaneous implantation of an osmotic pump with low dose of ISO and long duration (4 mg / kg, for 28 days). The phenotypes were determined by echocardiography, histopathological observation, immunofluorescence and Real-time PCR. Results The pathological phenotypes of rats were typical. The overall phenotypes included markedly increased heart size, heart weight to body weight ratio and heart wall thickness. The cell phenotypes included enlarged cardiomyocytes and severe myocardial fibrosis, myocardial fiber rupture and myolysis, mitochondria ridge disappearance and vacuolation, distortion of the Z-line, M-line and leap disk. The molecular phenotypes including increased expression of ANP and BNP. Conclusions The rat model established in this study exhibited typical CH phenotypes. This method is stable and easy to replicate and this model can be used for scientific research such as for gene function analysis and relevant drug screening.

Abstract: Objective To investigate the effect of atorvastatin on myelin repair and the RhoA/ Rock1 pathway in mice with autoimmune encephalomyelitis (EAE). Methods MOG35-55 immunization was used to establish an EAE mouse model. The mice were randomly divided into the control group, model group, atorvastatin group, high fat diet group and high fat diet+atorvastatin group ( n= 6 per group). The atorvastatin was administered to each mouse daily by 0. 5 mL suspension, for 28 consecutive days. Mice were scored for neurological function and clinical symptoms were observed. Hematoxylin-eosin ( HE ) staining, Luxol fast blue ( LFB ) staining, transmission electron microscopy and immunohistochemical staining method were used to detect inflammation and demyelination and remyelination of the spinal cord tissue of each group of mice. The expression of tumor necrosis factor-α (TNF-α), interleukin-6 ( IL-6) and nitric oxide (NO) in serum was detected by enzyme linked immunosorbent assay (ELISA); protein immanoblotting assay(Western blot) method was used to detect the expression of Ras homologous gene family member A (RhoA) and Rho associated protein kinase 1 (ROCK1) in brain tissue. Real-time fluorescence quantitative PCR (qRT-PCR) was used to detect the expression of chondroitin sulfate proteoglycan ( NG2) and myelin basic protein ( MBP) in spinal cord and RhoA and Rock1 mRNA expression in brain tissue. Results Compared with the control group, the model group showed more inflammatory cell infiltration, marked demyelination, partial myelination disintegration, breakage and demyelination; TNF-α, IL-6 and NO in serum and the expression of RhoA, Rock1 protein and mRNA in brain tissue were significantly increased, while the expression levels of NG2 and MBP protein and mRNA in spinal cord tissue were significantly decreased (P<0. 01). Compared with the model group, the atorvastatin group showed significant improvement in inflammatory cell infiltration and demyelination, significantly decreased TNF-α, IL-6 and NO in serum, expression of RhoA and Rock1 protein and mRNA in brain tissue and increased expression of MBP, NG2 protein and mRNA in brain tissue (P< 0. 05). The high fat diet + atorvastatin group showed significantly decreased neurological function scores, brain tissue RhoA and Rock1 expression and significantly increased NG2 mRNA expression. Conclusions Atorvastatin improved inflammatory cell infiltration and demyelination in EAE mice and reduced neurological function scores in EAE mice on a high fat diet. The mechanism of action may be related to the regulation of the RhoA/ Rock1 pathway to improve the degree of demyelination and thus exert a therapeutic effect on EAE mice.

Abstract: Objective To investigate the protective effect of naringenin on H₂O₂ -induced oxidative damage of human retinal pigment epithelial (RPE) cells via the miR-34a / silent information regulator 1( SIRT1) axis. Methods MTT assay was used to detect the effect of naringenin at different concentrations on the survival rate of ARPE-19 cells treated with H₂O₂ , and the appropriate naringenin concentration for subsequent experiments was identified. ARPE-19 cells in logarithmic phase were divided into the control group, H₂O₂ group (200 μmol / L), 20 μg / mL naringenin group, 20 μg / mL naringenin+mimics NC group and 20 μg / mL naringenin +miR-34a mimics group. RT-qPCR was used to detect the expression of miR-34a and SIRT1 mRNA, MTT assay and Annexin V-FITC/ PI double staining were used to detect cell survival and apoptosis, respectively. A fluorescence probe was used to detect the level of ROS, and a biochemical method was used to detect the activity of SOD and levels of MDA and GSH. JC-1 method was used to detect the mitochondrial membrane potential (MMP), and Western blot was used to detect the proteins expression of SIRT1 and Bcl-2, Bax and Caspase-3. Results The expression of miR-34a, apoptosis rate, contents of ROS and MDA and expression of Bax and Caspase-3 in ARPE-19 cells were significantly increased in the H₂O₂ group compared with those in the control group (P< 0.05). The expression of SIRT1 mRNA, survival rate of APRE-19 cells, contents of SOD and GSH, level of MMP, expression of SIRT1 and Bcl-2 were significantly decreased in the H₂O₂ group compared with those in the control group (P< 0.05). Naringenin improved the damage of ARPE-19 cells induced by H₂O₂ , down-regulated the expression of miR-34a, decreased the contents of ROS, MDA, Bax and Caspase-3 (P<0.05), up-regulated the expression of SIRT1, MMP and Bcl-2 and increased the activities of GSH and SOD compared with effects in the H₂O₂ group (P<0. 05). Up-regulation of miR-34a expression in ARPE-19 cells reversed the protective effect of naringenin on H₂O₂ -induced oxidative damage in RPE cells. Conclusions Naringenin down-regulates miR-34a, promotes the expression of SIRT1, inhibits the apoptosis of RPE cells and protects RPE cells from oxidative damage induced by H₂O₂ .

Abstract: Objective To investigate the effect of honokiol (HNK) on immune imbalance and lung function in chronic obstructive pulmonary disease (COPD) mice and to investigate whether the Notch signaling pathway mediates this process. Methods BALB/ c mice (male, 6~ 8 weeks old) were randomly divided into three groups: normal control group (Normal), COPD group and COPD+HNK group ( n= 10 mice per group). A mouse model of COPD was induced by cigarette smoke, and HNK (10 mg / kg) was intraperitoneally injected into the COPD+HNK group every other day for 30 days. The French EMKA GYD-003 animal lung function test system was used to detect the peak inspiratory flow rate (PIF) and peak expiratory flow rate (PEF). Hematoxylin-eosin (HE) staining was used to evaluate the pathological changes of lung tissue. Flow cytometry was used to detect the ratio of Th1 / Th2 and Th17 / Treg subgroups of mouse spleen T cells. Western blot was used to examine the protein expression of Notch 1 / 2 / 3 / 4, Hes1, Hes5 and Hey1 in T cells. ELISA was used to detect the levels of serum IFN-γ, IL-4, IL-17 and IL-10 in mice. Results The PIF and PEF of the COPD+HNK group mice were significantly increased compared with result in the COPD group (P<0. 05). In addition, the lung tissue lesions of the mice in the COPD+HNK group were reduced, the inflammatory cell infiltration was reduced, the number of alveoli increased and the alveolar cavity was reduced compared with result in the COPD group. Compared with the COPD group, the COPD+HNK group mice showed significantly reduced Th1 percentage, Th1 / Th2 ratio, Th17 percentage and Th17 / Treg ratio (P<0. 05). In addition, the relative expression levels of Notch1, Notch2, Notch3, Notch4, Hes1, Hes5 and Hey1 in the spleen T cells of the COPD+HNK group mice were significantly reduced (P<0. 05). The levels of IFN-γ and IL-17 in the serum of the COPD+HNK group were significantly reduced (P<0. 05), while the levels of IL-4 and IL-10 were significantly increased (P<0. 05). Conclusions HNK inhibits activation of the Notch signaling pathway of T cells in the spleen of COPD mice, thereby correcting the imbalance of Th1 / Th2 and Th17 / Treg cells in COPD mice and improving lung function.

Abstract: Objective To compare the effects and mechanisms of the ginsenosides Rg1, Rb1 and Rg1+Rb1 on improving spatial and non-spatial learning memory in a scopolamine-induced mouse model for cognitive impairment. Methods A scopolamine-induced cognitive impairment mouse model was established, and the effects of ginsenoside Rg1 or Rb1(60 μmol / kg) and Rg1+Rb1(30 μmol / kg each combined) on behaviors were observed by using object cognition experiments. Liquid chromatography-mass spectrometry-mass spectrometry will be used to determine neurotransmitter levels in mice, while colorimetric methods will be used to determine oxidative stress levels. Results Compared with the control group, the model mice showed severe impairment on both short-term spatial learning memory and non-spatial learning memory (P<0.001). Huperzine A and ginsenoside Rg1, Rb1 and Rg1+Rb1 administration significantly reversed the short- term non-spatial learning memory impairment in the model mice, but the effect of ginsenoside Rg1+Rb1 on improving short- term spatial learning memory was weaker than that of ginsenoside Rb1 (P<0.01). Hippocampal Ach, 5-HT and Glu levels were decreased in the model mice compared with controls. Administration of Huperzine A or ginsenosides Rg1, Rb1 and Rg1+Rb1 significantly increased hippocampal Ach, 5-HT and Glu levels in the model mice. Serum oxidative stress levels were significantly increased in the model mice compared with controls. Administration of ginsenoside Rg1, Rb1 and Rg1+ Rb1 significantly increased serum SOD, CAT and GSH activity and significantly decreased MDA levels in the model mice. Although ginsenoside Rg1 + Rb1 was weaker than ginsenoside Rb1 in regulating GSH activity ( P< 0. 01, P< 0. 05), ginsenoside Rg1+Rb1 was stronger than ginsenoside Rg1 and Rb1 in the ability to regulate MDA. Conclusion Although half dosage combination of ginsenoside Rg1 +Rb1 exhibited decline in the ability to improve spatial short-term learning memory. However, ginsenosides Rg1, Rb1 and Rg1+Rb1 were comparable in their ability to improve short-term non-spatial learning memory impairment. The differences may be related to the dose and the ability of different ginsenosides on the regulation of neurotransmitters and oxidative stress levels in the brain.

Abstract: Objective To explore establishment method of three-dimensional modeling and 3D printing of pulmonary in minipigs, and apply the constructures to clinical trials. Methods Four Bama minipigs were subjected to general anesthesia and CT angiography. Imaging data were reconstructed by MIMICS software into tissues of pulmonary and used to print the indicated structures of pulmonary vessels and bronchus using a 3D printer. Results The three- dimensional model from the CT angiography data revealed three to four levels of anatomical structure of pulmonary vessels and bronchus, lobar fissure and partial intersegmental planes. The 3D model, rotating and auto-zooming is consistent with the pulmonary tissue. Conclusions Constructures of pulmonary vessels, bronchus and whole pulmonary tissue in Bama minipigs could be reconstructed by three-dimensional reconstruction and 3D printing technology, which provide reference for comparative medical research and have been materinals for thoracic surgery training.

Abstract:The small animal neurobehavior experiment platform has been the most basic supporting condition in the field of neuroscience and brain science. This paper systematically discusses the planning and design principles and construction requirements of the small animal neurobehavior experiment platform, including general principles for design and construction, platform layout and function division, the corresponding supporting facilities and equipment and the construction requirements for the small animal neurobehavior experiment platform. These discussions help provide planning and design references and construction specifications for the construction of specialized small animal neurobehavior laboratories.

Abstract:Laboratory animal science is a supporting discipline for many fields such as life science, medicine and pharmacy. The level of employees from laboratory animal science is not only related to the standardized development of laboratory animal industry, but it also affects the scientific and technological innovation and industrial development of biomedicine and other fields and is involved in biosafety and social civilization. Therefore, the training and qualification system of employees in laboratory animal science is very important. We investigated the training processes of laboratory animal employees in Europe, the United States, Japan and China, including the standards, classification, grade, training content and level evaluation. The training system for laboratory animal technicians and doctors is relatively developed, while the training system of domestic laboratory animal managers needs to be established. However, there is a general lack of training and evaluation systems for laboratory animal researchers worldwide. Therefore, the establishment of an evaluation system suitable for the self-development of laboratory animal researchers is analyzed and suggested.

Abstract:Prostate cancer (PCa) is the second most common malignant tumor among men worldwide and has an increasing incidence. The main characteristic of PCa is heterogeneity, which includes not only variations of tumor histological characteristics among patients, but also differences in growth, invasion and metastasis speed of tumor cells in the same patient. Recent studies showed that the JARID1D demethylase, which is encoded from the Y chromosome, specifically binds to the promoters of genes related to invasion and metastasis, such as MMP1, MMP2 and MMP3, and demethylate at the promoter through a gene activation marker such as H3K4, so as to inhibit the production of some invasive compounds and reduce the invasive ability of prostate cancer. Meanwhile, knocking down the expression of demethylase JARID1D will improve the metastatic potential of prostate cancer and even promote multiple organ metastasis, including bone metastasis.In this review, we summarize the recent progression on the research on the JARID1D demethylase. We discuss its structure and the enzymatic and regulatory mechanisms, and we review the role of JARID1D in the invasion and metastasis of prostate cancer. We also explore novel intervention targets for PCa therapy.

Abstract:Trace amine-associated receptor 1 (TAAR1) is a new signal in neuropsychiatric research and plays an important physiological role in the central nervous system. Various reports have shown that the role of TAAR1 is closely related to trace amines and monoamine neurotransmitters. We discuss the research on TAAR1 in recent years from the aspects of TAAR1 expression, related ligands, mechanism pathway and the relationship with monoamine neurotransmitters. TAAR1 regulates dopaminergic, serotoninergic and glutamatergic neurons in the central nervous system and thus affects the levels of related substances inside and outside the cell. TAAR1 agonists also show great potential for promoting the cognitive function in pharmacological experiments. Targeting this receptor shows increasing advantages and potential for use in neuropsychiatric diseases.

Abstract:Pyroptosis is a novel type of programmed cell death characterized by the formation of micropores in the cell membrane by activated gasdermin D, which changes the osmotic pressure between the inside and outside of the cell. This eventually swells and ruptures the cell, and releases a large number of inflammatory factors and cytoplasmic contents, thereby participating in the inflammatory immune response. Studies have shown that pyroptosis is closely related to the occurrence and development of liver damage, and excessive pyroptosis aggravates liver damage. This article mainly reviews the different activation pathways of pyroptosis and its mechanisms of action in the liver injury microenvironment.

Abstract:Microbial keratitis is a common ocular disease worldwide and is an important cause of vision loss and blindness. A comprehensive understanding of the pathogenesis of microbial keratitis is required for the establishment of animal models of related diseases. These models play an important role in studying the immune response and infection mechanism of host infections and drug development, and provide a scientific evidence for the selection of clinical treatment strategies and pursuing basic research。 Here we summarize the animal models and the pathogenic mechanism of infectious keratitis to provide comprehensive understanding of the current research on these models.

Abstract:The nuclear factor erythroid-2-related factor2 (Nrf2) / antioxidant response element (ARE) signaling pathway is an essential antioxidant pathway regulated by redox. Activation of this pathway plays an important role in regulating oxidative stress, maintaining mitochondrial function, inhibiting ferroptosis in dopaminergic neurons and ptotecting them against oxidative damage. Targeting this pathway for the treatment of Parkinson’ s disease ( PD) has become a research focus. In this review, we summarize and analyze the current research on the Nrf2-ARE pathway, including the mechanisms, function and relation with PD. These insights may help further clarify the relationship between Nrf2-ARE pathway and PD and aid in developing new ideas for new PD drugs targeting the Nrf2-ARE pathway.