Abstract: Objective To compare the advantages and disadvantages of two high-glucose-induced hippocampal neuron models, and explore their application in different situations. Methods Primary hippocampal neurons and HT-22 hippocampal neuron cell lines were cultured in vitro and divided into control and high glucose groups. Neurons were purified and cell viability was measured. The effect of transfection reagents on cell viability and transfection efficiency was determined and flow cytometry was used to observe cell apoptosis. Western blot was used to detect apoptotic protein expression. Results The purity of primary hippocampal neurons was > 85%. Two high-glucose-induced neuronal cell models were successfully modeled. The high-glucose action time was 48 hours, the activity of primary neurons was stable at 80%, and the activity of HT-22 cells was >95%. The liposome transfection reagents caused damage in the two cell models. LipoRNAiMax was less toxic to HT-22 cells, which also had a high transfection efficiency. The two models showed significant apoptosis, compared with the primary neuron control group, the apoptosis rate of the primary neuron high glucose group increased, compared with the HT-22 control group, the HT-22 high glucose group increased cell apoptosis ( P< 0. 05). Compared with HT-22 high glucose group, the apoptotic rate of primary neurons high glucose group was higher, the expression of apoptotic protein Bcl-2 was decreased, and the expression of Bax was increased in primary neurons ( P< 0. 05). Compared with HT-22 control group, there was no difference in the expression of Bax in HT-22 high glucose group . Conclusions The two high-glucose-induced hippocampal neuron cell models had different advantages and disadvantages. The choice of cell model should be considered based on actual conditions.

Abstract: Objective To investigate the expression of rpl15 in zebrafish. Methods The NCBI and Ensemble databases were used to analyze the co-collinearity of the rpl15 gene and the sequence similarity of rpl15 protein. MEGA X software was used to align rpl15 in different organizations. The mRNA expression of rpl15 was detected in whole embryos by in situ hybridization with an rpl15 antisense RNA probe, and the expression of rpl15 protein in 24, 48, and 72 hpf zebrafish embryos was detected by western blotting. Results The rpl15 gene is relatively conserved during evolution. A pCS2⁺ -rpl15 recombinant plasmid was constructed, and in situ hybridization result showed that at 24 hpf, rpl15 was widely expressed in most cells of zebrafish. At 48 hpf, rpl15 expression was highest in the central nervous system and it was also present in the pancreas. At 72 hpf, rpl15 expression was still present in the posterior brain, as well as the pancreas, liver, and intestine. The relative protein expressions of rpl15 in 24, 48, and 72 hpf zebrafish embryos increased with increasing time. Conclusions Changes in the expression sites and expression levels of rpl15 in zebrafish during development were systematically observed, which provide the experimental basis for establishing a model of rpl15 deletion in zebrafish.

Abstract: Objective To establish a stable method for the isolation, culture, and characterization of mouse lung- resident mesenchymal stem cells, which will then be used to study lung repair and regeneration mechanisms. Methods Mouse lungs were obtained via germ-free procedures and were mechanically minced and / or digested with collagenase. Cell morphology was observed by phase-contrast microscopy, cell surface markers were detected by flow cytometry, and cells were induced to differentiate into adipocytes or osteoblasts. Results We successfully isolated and cultured mouse lung- resident mesenchymal stem cells. FACS analysis demonstrated high expressions of Sca-1, CD90, CD29, and CD44, and low expressions of CD31 and CD45. The lung-resident stem cells differentiated into adipocytes or osteoblasts. Conclusions We isolated cells that expressed mesenchymal stem cell markers and had multi-directional differentiation ability.

Abstract: Objective To explore the regulatory effect of Cosentyx on skin inflammation and autophagy in psoriasis mice (IMQ-induced) through the C5a / C5aR1 pathway. Methods Twenty-eight 8-week-old BALB/ c male mice were assigned to three groups of nine mice each: Blank, Psoriasis-Model, and Cosentyx-Treated Groups. All except the Blank Group received IMQ and the Cosentyx-Treated Group was treated with Cosentyx (subcutaneous injection, 4. 5 mg / kg twice a day on days 1, 6, and 13). HE staining was used to observe the effect of Cosentyx on pathological damage in the skin of psoriasis mice. ELISA was used to measure the secretion of the proinflammatory cytokines IL-4, IL-8, TNF-α, and IL-1β in psoriasis mouse skin. Spectrophotometry was used to observe the activity of medullary peroxidase (MPO) in mouse skin. Western blot analyses were used to measure Beclin 1 expression and LC3-II/ LC3-I values. Immunohistochemistry analyses were performed to detect the expressions of C5a, C3, C5aR1, and C1qB in skin. Results Cosentyx inhibited the expressions of IL-4, IL-8, TNF-α, IL-1β, and MPO in dermal tissues, improved Beclin 1 expression and the LC3-II/ LC3- I ratio, and downregulated the expressions of C1qB, C3, C5a, and C5aR1. Conclusions Cosentyx inhibited the C5a / C5aR1 pathway, regulated the expression of inflammatory cytokines in psoriasis skin, and slowed psoriasis inflammation. Cosentyx enhanced autophagy in psoriasis skin tissues but we did not determine whether Cosentyx controlled autophagy through the C5a / C5aR1 pathway. Therefore, the mechanism requires further study.

Abstract: Objective To explore the effects of Sijunzi Decoction containing serum on the proliferation, migration, invasion, and epithelial mesenchymal transition of ovarian cancer cells, and the mechanism involved. Methods Human ovarian cancer cells (SKOV3) and human ovarian epithelial cells were cultured in vitro and randomly divided into blank control, sunitinib, and Sijunzi Decoction I, II, and III groups. The methyl thiazolyl tetrazolium assay was used to detect the proliferation of SKOV3 cells and human ovarian epithelial cells. The migration and invasion abilities of SKOV3 cells were examined using the scratch test and transwell test. The protein expressions of E-cadherin, N-cadherin, vimentin, RAS homolog gene family member A (RhoA), Ras-related C3 botulinum toxin substrate 1 (Rac1), and cell division cycle 42 (Cdc42) in SKOV3 cells were detected by western blotting. In addition, the mRNA expressions of RhoA, Rac1, and Cdc42 in SKOV3 cells were detected by real-time quantitative PCR ( qRT-PCR). Results There was no significant difference in the survival rate of human ovarian epithelial cells among the groups (P> 0. 05). Compared with the blank control group, the survival rate, wound healing rate, invasion number, protein expressions of N-cadherin and vimentin, and mRNA and protein expressions of RhoA, Rac1, and Cdc42 in SKOV3 cells in the sunitinib group were significantly lower (P<0. 05), and the protein expression of E-cadherin was significantly higher (P<0. 05). The survival rate, wound healing rate, invasion number, protein expressions of N-cadherin and vimentin, and mRNA and protein expressions of RhoA, Rac1, and Cdc42 in SKOV3 cells in the Sijunzi Decoction I, II, and III groups were decreased (P<0. 05), and the protein expression of E-cadherin was increased (P< 0. 05) dose-dependently. There was no significant difference in these indexes between the Sijunzi Decoction III and sunitinib groups ( P> 0. 05 ). Conclusions Sijunzi Decoction containing serum inhibits the proliferation, migration, invasion, and epithelial mesenchymal transition of human ovarian cancer cells, which may be related to inhibition of the RhoA/ Rac1 / Cdc42 signaling pathway activation.

Abstract: Objective CRISPR/ Cas9 and Cre-loxP were used to construct the conditional knockout of taurine transporter (TauT) in the central nervous system of rats. The mitochondrial mtDNA and mitochondrial respiratory chain enzyme activities in brain tissues were studied. Methods CRISPR/ Cas9 and Cre-loxP techniques were used to obtain heterozygous rats (TauT^{loxP / WT} ) with loxP at both ends of exon 5 of the TauT gene. The obtained TauT^{loxP / WT} rats were mated with Nestin-Cre rats. After breeding and identification, neural-specific TauT gene knockout rats ( TauT^{loxP / loxP / Cre+} ) were obtained. The gene and protein expressions of TauT^{loxP / loxP / Cre+} rats were detected by Real-time PCR, Western blot, and immunohistochemistry. The morphology of brain tissue was observed by hematoxylin-eosin staining. The mtDNA copy number and mitochondrial respiratory chain enzyme ( I/ II/ III/ IV/ V) activity in brain tissue were examined. Results Compared with wild-type rats, TauT gene and protein expressions in TauT^{loxP / loxP / Cre+} rat brain tissues were significantly decreased, and the TauT gene was successfully knocked out in the central nervous system indicating the knockout model was successfully constructed. Hematoxylin-eosin staining showed that the number and density of brain cells were decreased in TauT^{loxP / loxP / Cre+} rats and cytopathic changes more obvious in the brains of old TauT^{loxP / loxP / Cre+} rats. In addition, compared with wild-type rats, the activities of mitochondrial respiratory chain complex enzymes Ⅰ, Ⅲ, Ⅳ, and Ⅴ were significantly decreased, but the copy number of mtDNA was significantly increased. Conclusions The model of TauT gene knockout in the central nervous system of rats was successfully constructed using CRISPR/ Cas9 and Cre-loxP technology. The effects of TauT knockout in the central nervous system on brain tissues, respiratory chain enzymes, and mtDNA of mitochondria were verified, providing a new model platform for the study of the molecular mechanisms of taurine and TauT in brain tissues.

Abstract: Objective To explore the effects of salidroside ( SAL) on nuclear transcription factor-E2 related factor 2 / Kelch-like epichlorohydrin-related protein 1 ( Nrf2 / Keap1) signaling pathway and wound healing in rats with diabetic foot ulcer (DFU). Methods Diabetes was induced in rats by feeding of a high-fat and high-glucose diet and intraperitoneal injecting of streptozotocin (STZ), and the back of the foot was shaved and cut to the fascia to create an ulcer wound with an area of approximately 3 mm×7 mm to establish DFU rat model. The rats were randomly allocated to a DFU model group; Sal-L (0. 1 g(kg·d)), Sal-M (0. 2 g / (kg·d)), Sal-H (0. 3 g( kg·d)) groups, metformin group (MET, 0. 65 g / (kg·d)), and set normal blood glucose wound rats as the control group (NC group), and all were gavaged daily for 2 weeks. The body mass and concentration of fasting-blood glucose (FBG) of all the rats were measured on the 7th and 14th days of treatment; the expression of CD34 was assessed by immunohistochemistry; the microvascular density (MVD) of the wounds was calculated; the levels of malondialdehyde (MDA) and superoxide dismutase (SOD) concentrations were measured biochemically, and the expression of Nrf2 and Keap1 proteins in the wound tissue was measured by Western blot. Results Prior to the start of treatment, there was no significant difference in the body masse between the groups, while the FBG of the DFU, Sal-L, Sal-M, Sal-H, and MET groups was higher than that of the NC group (P<0. 05). On the 7th and 14th day of treatment, the body mass, FBG, MDA content, and Keap1 protein expression in the DFU, Sal-L, Sal-M, Sal- H, and MET groups were higher than those in the NC group (P<0. 05); and the wound healing rate, CD34 positive cells, MVD, SOD activity, and Nrf2 protein expression were significantly lower (P<0. 05). The body mass, FBG, MDA content, and Keap1 protein expression in the Sal-L, Sal-M, Sal-H, and MET groups were lower than those in the DFU group (P< 0. 05); and the wound healing rate, CD34 positive cells, MVD, SOD activity, and Nrf2 protein expression were significantly higher (P<0. 05). However, there were no significant differences between the Sal-L and MET groups (P> 0. 05). Conclusions Sal may increase the antioxidant capacity and promote wound healing in rats with DFU via the Nrf2 / Keap1 signaling pathway.

Abstract: Objective To investigate the effects of prostaglandin E1 ( PGE1) on liver function in rats with fulminant hepatic failure ( FHF), and to explore its regulatory effects on the eukaryotic translation-initiation factor 2α (eIF2α) / activating transcription factor 4 (ATF4) / C/ EBP homologous protein (CHOP) pathway. Methods Overall, 90 specific pathogen-free Sprague-Dawley rats were divided into control, model, positive control, low-, medium-, and high- dose PGE1 groups according to the random number table method . Except for the control group, all rats were intraperitoneally injected with D-galactosamine (D-GalN)-lipopolysaccharide (LPS) to establish the FHF rat model, and the control group received an intraperitoneal injection of the same volume of normal saline. At 6 hours after modeling, the positive control group and low-, medium-, and high-dose PGE1 groups were administered a tail vein injection of 1. 36 mg / kg hepatocyte growth promoting factor and 12. 5, 25, or 37. 5 μg / kg PGE1, respectively, once a day for 3 consecutive days. The control group and the model group were administered a tail vein injection of the same volume of normal saline. The rats were euthanized at 72 hours after modeling and abdominal aorta blood was collected. The serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and total bilirubin (TBIL) were measured. Liver tissues were dissected and stained with hematoxylin and eosin ( HE) to observe pathological changes. mRNA and protein levels of eIF2α/ ATF4 / CHOP / caspase-3 were detected by real-time fluorescence quantitative PCR (qRT-PCR) and Western blot was used to measure phosphorylated-eIF2α ( p-eIF2α) protein levels. Results Compared with the control group, hepatocytes in the model group showed extensive degeneration and focal necrosis, and the central venous was damaged. The levels of ALT, AST, and TBIL in serum, mRNA levels of eIF2α, ATF4, CHOP, and caspase-3, and protein levels of p-eIF2α/ eIF2α, ATF4, CHOP, and caspase-3 in liver tissues were higher (P< 0. 05). Compared with the model group, the damage to hepatocytes and the number of necrotic cells were decreased in the positive control, low-, medium-, and high-dose PGE1 groups. The levels of ALT, AST, and TBIL in serum, mRNA levels of eIF2α, ATF4, CHOP, and caspase-3 and protein levels of p-eIF2α/ eIF2α, ATF4, CHOP, and caspase-3 in liver tissues were lower (P< 0. 05). With an increase in PGE1 dosage, the levels of ALT, AST, and TBIL in serum, mRNA levels of eIF2α, ATF4, CHOP, and caspase-3 and protein levels of p-eIF2α/ eIF2α, ATF4, CHOP, and caspase-3 in the liver tissues of low-, medium-, and high-dose PGE1 groups were decreased (P< 0. 05) dose-dependently. Compared with the positive control group, the levels of ALT, AST, and TBIL in serum, mRNA levels of eIF2α, ATF4, CHOP, and caspase-3 and protein levels of p-eIF2α/ eIF2α, ATF4, CHOP, and caspase-3 in the liver tissues of the low- and medium-dose PGE1 groups were higher (P< 0. 05). However, there was no significant difference in the levels of ALT, AST, and TBIL in serum, mRNA levels of eIF2α, ATF4, CHOP, and caspase-3 and protein levels of p-eIF2α/ eIF2α, ATF4, CHOP, and caspase-3 in liver tissues between the positive control group and the high-dose PGE1 group ( P> 0. 05). Conclusions PGE1 may reduce the apoptosis of rat hepatocytes and protect the liver by inhibiting the expression of the eIF2α/ ATF4 / CHOP pathway, which may be a potential therapeutic target for FHF.

Abstract: Objective To explore the role and underlying mechanisms of miR-433-3p in hydrogen peroxide (H₂O₂ )-induced injury to H9c2 cardiomyocytes. Methods An oxidative stress injury model of H9c2 cardiomyocytes was established. H9c2 cardiomyocytes were transfected with miR-433-3p mimics, miRNA mimic negative control (miR-NC), pcDNA-NC, and a MAPK8 overexpression plasmid (pcDNA-MAPK8) and treated with H₂O₂ . H9c2 cells were divided into Control, H₂O₂ , H₂O₂+ miR-NC, H₂O₂+ miR-433-3p mimic, H₂O₂+ miR-433-3p mimic + pcDNA-NC, and H₂O₂+ miR- 433-3p mimic + pcDNA-MAPK8 groups. The mRNA expressions of miR-433-3p and MAPK8 in H9c2 cells were detected by qRT-PCR assay. Cell viability and the amount of lactate dehydrogenase (LDH) released were detected by MTT assay and ELISA kits, respectively. Cell apoptotic-related protein expressions of Bax, Bcl-2, caspase-3, and cleaved caspase-3 were measured by Western blot analysis. The luciferase reporter assay was performed for testing the targeting relationship between miR-433-3p and MAPK8. Results Compared with the control group, the expression of miR-433-3p was lower in H₂O₂ -induced H9c2 cardiomyocytes. Compared with the H₂O₂ + miR-NC group, miR-433-3p overexpression significantly reduced the amount of LDH released and enhanced cell viability. In addition, compared with the H₂O₂ + miR-NC group, miR-433-3p overexpression significantly decreased the expressions of the pro-apoptotic proteins Bax and cleaved caspase-3, but increased the expression of the anti-apoptotic protein Bcl-2. The luciferase reporter assay showed that miR-433-3p directly targeted MAPK8 and negatively regulated the expression of MAPK8. Overexpression of MAPK8 reversed the inhibitory effects of miR-433-3p overexpression in H₂O₂ -induced H9c2 cell injury and apoptosis. Conclusions miR-433- 3p has a protective role in cardiomyocyte injury induced by H₂O₂ through the negative regulation of MAPK8.

Abstract: Objective To study the effects of different doses of isoproterenol ( ISO) on cardiac function and pathological morphology in rats. Methods Sprague-Dawley rats were randomly divided into Control, low-dose model (ISO 25 mg / kg), medium-dose model (ISO 50 mg / kg), and high-dose model (ISO 100 mg / kg) groups. In the model group, different doses of ISO were injected subcutaneously at multiple points in the neck for two consecutive days whereas the Control group received the same volume of saline. Changes in heart rate, QRS interval, duration and amplitude of P-waves were detected by electrocardiogram (ECG). The myocardial infarct size was detected by TTC staining and the pathological morphology of myocardial tissues was observed by HE staining 24 hours after the last administration. Results Compared with the Control group, the heart and left ventricular weights of rats in different dose model groups were significantly increased (P< 0. 01) and the ECG of rats showed that the P-wave duration in the high-dose model group was increased (P< 0.01), the P-wave amplitude in the low-dose and high-dose model groups was increased (P< 0.05, P< 0.01, respectively) and arrhythmia was present. TTC staining and HE staining showed pathological changes related to myocardial injury. Conclusions Different degrees of damage were observed in myocardial tissues of the model groups and the most serious myocardial injury was observed in the high-dose model group. This study provides a basis for animal model development and research of the mechanisms of ischemic / infarct heart disease.

Abstract: Objective To study the protective effect of safflower yellow (SY) in mice with diabetic nephropathy (DN) induced by streptozotocin (STZ). Methods DN was induced by the intraperitoneal injection of STZ (50 mg / kg) for 5 consecutive days. Thirty-six male C57 BL/ 6J mice with DN were randomly allocated to a model group, and SY-10 mg / kg, SY-30 mg / kg, and SY-90 mg / kg groups. The three experimental groups were administered SY once daily for 10 weeks. Their blood glucose and body mass were monitored, and blood urea nitrogen ( BUN) and serum creatinine ( Scr) were analyzed. Renal pathology was assessed using hematoxylin and eosin-stained sections. The protein expression levels of PKC, P-Raf, Raf, P-ERK, ERK were measured using Western blot analysis. The contents of GSH, MDA, and SOD, and the expression levels of TNF-α, IL-6, and IL-1β were measured using ELISA kits. Results Compared with a control group, the food and water consumption and blood glucose concentration were higher, and the body mass was lower in the model group. The body mass, blood glucose, BUN, and Scr were higher in all the treatment groups, but the glomerular hypertrophy, basement membrane thickening, and vacuolar degeneration of renal tubules were ameliorated. The contents of SOD and GSH were higher, whereas that of MDA was lower, and the expression levels of proinflammatory factors were lower in the treatment groups. Finally, the protein expression of PKC, P-Raf, and P-ERK was lower in the SY-30 and SY-90 groups. Conclusions SY may ameliorate inflammation and oxidative stress in DN, which might be mediated via the PKC/ Ras-Raf-MEK-ERK signaling pathway.

Abstract: Objective To determine the effects of rixolipite granules on renal calcium oxalate calculi and protein kinase C (PKC)-nuclear factor erythroid-2-related factor 2 (Nrf2) signaling to antioxidant response elements (AREs). Methods Thirty-two specific pathogen-free Sprague Dawley rats were randomly allocated to four groups ( n= 8 each): a control group, a model group, a treatment group, and an inhibitor group. All of the rats except the controls were administered ethylene glycol and ammonium chloride in their diet to induce urinary calcium oxalate calculus formation within 28 days. The treatment group was also administered 10. 0 g / kg Lengzhu Paishi granules, and the inhibitor group was administered 30 mg / kg r031-8220 once daily by gavage for 28 days. Afterward, 24 h urine volume, urine pH, urinary oxalic acid (Ox) concentration, the circulating Ca²⁺ and Mg²⁺ concentrations and the 24 h urinary output of each, blood urea nitrogen (BUN), and circulating creatinine (Cr) concentrations were measured. The protein expression of PKC, Keap1, Nrf2 was characterized using von Kossa staining and Western blot. Results The model group had significantly lower 24 h urine volume, urine pH, circulating Mg²⁺ , urinary Mg²⁺ , and renal superoxide dismutase activity than the control group; and the Ox, circulating and urinary Ca²⁺ , renal malondialdehyde concentration, reactive oxygen species fluorescence intensity, and PKC, Keap1, and Nrf2 protein expression were significantly higher (P<0. 05). Lengzhu Paishi granule treatment significantly ameliorated all these effects (P<0. 05). There was no significant difference between the two groups (P>0. 05). Conclusions Lengzhu Paishi granules prevent the pathological changes associated with renal calcium oxalate calculus formation in rats, which may be mediated through the activation of the antioxidant signaling pathway PKC- Nrf2 / ARE and a reduction in oxidative stress.

Abstract: Objective To explore the mechanism of ropivacaine induced apoptosis in a human colorectal cancer (CRC) SW620 cell line via the mitochondrial pathway. Methods Human CRC SW620 cells were cultured in vitro and treated with ropivacaine. The viability of cancer cells was determined by CCK-8 assay. CRC cells were divided into CRC cell, low-dose, medium-dose, and high-dose ropivacaine groups. Referring to the CCK-8 assay result , CRC cells in the low-dose, medium-dose, and high-dose ropivacaine groups were treated with 20, 50, and 100 μg / mL ropivacaine, respectively. The mitochondrial membrane potential (MMP) in each group was detected by flow cytometry. The expression of apoptosis proteins (Bcl-2, Bax, caspase-3, caspase-9) was detected by western blot. The cell cycle and apoptosis of CRC SW620 cells were determined by flow cytometry. Results The CCK-8 assay showed that with an increase in ropivacaine dose, the inhibition rate of human CRC SW620 cells was significantly increased, and the lethal dosage 50 (LC50 ) was approximately 69. 36 μg / mL. The apoptosis rate in the CRC cell group was 1. 52 ± 0. 11%, which was significantly lower than that in the low-dose, medium-dose, and high-dose ropivacaine groups ( 35. 91±5. 69%, 46. 27± 6. 57%, 69. 36±8. 01%, respectively; F= 559. 203, P<0. 001). Compared with the CRC cell group, the MMP, ratio of cells in G2 / M phase, ratio of cells in S phase, and the relative expression level of Bax protein were significantly and dose- dependently decreased in each group treated with ropivacaine (P<0. 001), whereas the ratio of cells in G0 / G1 phase, and the relative expression levels of Bcl-2, caspase-3, and caspase-9 proteins were significantly and dose-dependently increased (P<0. 001). Conclusions Ropivacaine promoted the apoptosis of human CRC SW620 cells via the mitochondrial pathway and the action mechanism may involve signal transduction related to caspase-3 and Bcl-2.

Abstract: Objective To investigate the mechanism whereby Wenyanghuayin decoction ameliorates airway remodeling in rats with bronchial asthma and syndrome of cold fluid accumulation, focusing on the ERK1 / 2 and p38 MAPK signaling pathways. Methods Sprague Dawley rats were randomly allocated to normal, model, control, and experimental groups (n= 15 each). Ovalbumin sensitization, stimulation, and atomization were used to induce bronchial asthma in the model rats, then iced water feeding was stimulated by “ cold drinking” and freezing in a refrigerator was stimulated by “ form cold” to model the syndrome of cold drink accumulating in the lung. Rats in the experimental and control groups were administered 30 mg / kg Wenyanghuayin decoction or rapamycin in physiological saline by gavage, respectively, and the normal and model groups were administered the same volume of normal saline for 22 consecutive days. A small and micro animal lung function analyzer was used to assess the lung function of the rats. TUNEL staining was used to detect cell apoptosis in lung tissue. ELISA kits were used to measure the serum concentrations of interleukin ( IL-6) and tumor necrosis factor-α (TNF-α). Western blot was used to measure the expression of p-ERK1 / 2, p-p38 MAPK, the apoptosis- related protein Bax, and Bcl2 in lung tissue. Results Compared with the normal group, the airway resistance during inhalation (Rinsp) and expiration (Rexp), the serum concentrations of IL-6 and TNF-α, the rate of apoptosis, and the expression of p-ERK1 / 2, p-p38 MAPK, and Bax were significantly higher, and the dynamic compliance ( Cdyn) and expression of Bcl-2 were significantly lower ( all P<0. 05) in the model group than in the control group. The Rinsp and Rexp, serum IL-6 and TNF-α, apoptosis rate, and expression of p-ERK1 / 2, p-p38 MAPK, and Bax were significantly lower; and the Cdyn and the expression of Bcl-2 were significantly higher than in the control and experimental groups (all P<0. 05). Conclusions In a rat model of airway remodeling during bronchial asthma and syndrome of cold fluid accumulation in the lung, Wenyanghuayin decoction significantly inhibits the release of proinflammatory factors and reduces lung cell apoptosis, which may be mediated via inhibition of ERK1 / 2 and p38 MAPK signaling pathways.

Abstract: Objective To confirm the performance of the pulsating vacuum sterilizer and its effect on SPF golden hamster cages and drinking water under specified loading and sterilization conditions. Methods The pulsating vacuum sterilization of different articles in the same load were performed by chemical and physical method with a professional temperature probe and biological indicator. First, a no-load pressure holding test and B-D test of the pulsating vacuum sterilizer and no-load heat distribution test were performed to confirm the performance of the sterilizer itself. Then, full-load heat distribution / heat penetration / microbial challenge, and asepsis tests were performed according to the specified loading method and sterilization conditions. Results The performance of the pulsating vacuum sterilizer was determined: vacuum holding pressure, B-D test, and no-load heat distribution test were all qualified. The test result of SPF golden hamster cages and drinking water subjected to full-load heat distribution / heat penetration / microbial challenge tests in accordance with specified loading method and sterilization conditions were qualified. After high pressure conditions, the sampling pads and drinking water were placed in culture medium for 14 days, but no bacterial colony growth was observed indicating the success of the sterility test. Conclusions SPF golden hamster cages and drinking water can be sterilized by pulsating vacuum sterilization under specified loading method and sterilization conditions.

Abstract:MicroRNAs (miRNAs) are a group of highly conserved non-protein-coding nucleotide sequences with a length of approximately 20~ 22 nucleotides. miRNAs were first discovered in Caenorhabditis elegans. Since then, research on the function and mechanism of miRNAs has gradually increased. To date, studies have shown that miRNAs are involved in lung growth and development, inflammatory responses and immune regulation, and are closely related to the occurrence, development, and outcome of respiratory diseases. Identifying the targets of miRNAs and using miRNA interference technology to explore related signal transduction pathways will help enhance our understanding of related diseases and provide a basis for clinical diagnosis and treatment. This article reviews the research background, formation mechanism, and biological function of miRNAs, as well as research and application progress in various respiratory inflammatory diseases. This will provide new ideas for the diagnosis and treatment of respiratory inflammatory diseases.

Abstract:Substance-related disorders ( SRDs) are a series of physical and mental disorders, involving drug abuse, medicinal side effects, and toxin exposure. SRDs, including alcohol- and drug-related disorders, have become a serious worldwide public health problem. Methyl-CpG-binding protein 2 (MeCP2), an important regulator in the central nervous system, has an important role in many biological functions, such as synaptic plasticity, neuron development, and adult brain function. Many studies have shown that MeCP2 is involved in several SRDs. MeCP2 exerts its regulatory effects on the transcription of genes leading to changes in hormone levels, inflammation, and synaptic plasticity. Generally, MeCP2 influences reward behavior, social behavior, cognitive behavior, and spatial memory. The regulatory mechanism of MeCP2 on SRDs is complex and is poorly understood. Here, we review the role of MeCP2 in SRDs, which will aid future studies of SRDs.

Abstract:Atherosclerosis is a chronic inflammatory disease caused by various pathogenic factors. Lipid metabolism disorders have a fundamental role in the pathogenesis of atherosclerosis. The liver is the largest metabolic organ in humans and has a key role in lipid metabolism by influencing fat production, fat decomposition, and the intake and secretion of serum lipoproteins. By targeting hepatic lipid metabolism, research and development studies have focused on novel lipid-lowering strategies. Here, we review novel approaches to target the regulation of liver lipid metabolism for the treatment of atherosclerosis, including new biomarkers, therapeutic targets, traditional Chinese medicine, and natural dietary supplements.

Abstract:Enhancer of zeste homolog 2 (EZH2), a histone methyltransferase and catalytic component of PRC2, catalyzes the tri-methylation of histone H3 at LYS27 ( H3K27me3 ) to regulate gene expression through epigenetic machinery, and is a member of the polycomb group of proteins. EZH2 is involved in the epigenetic inhibition of the expressions of numerous tumor suppressor genes, regulation of the cell cycle, promotion of cell proliferation, and cell invasion. The tumor microenvironment is related to the occurrence of tumors, tumor development, and prognosis. Recently, many studies have reported that EZH2 is expressed in a variety of immune cells and regulates the tumor microenvironment. It is also an essential component of immune responses and anti-tumor immunity. We summarize the function of EZH2 in different cell types and explore its potential as a tumor immunotherapy target.

Abstract:Parkinson’s disease (PD), the second most prevalent neurodegenerative disorder worldwide, lacks a cure. The discovery and evaluation of treatment method are dependent on nonhuman primate (NHP) models of PD. A reliable and valid animal model can contribute to understanding the pathogenesis, diagnosis, therapy, and drug discovery related to PD. Rodents and invertebrates are commonly used to establish PD models. However, Results using rodent and invertebrate models do not accurately represent the behavioral and pathological characteristics of human PD. NHPs are the closest animals to humans in terms of physiology, structure, and immunology, which makes them suitable for studies to understand the mechanisms of disease and establish new therapies. This article reviews the progression of PD models in NHPs, thereby providing a reference for PD model establishment.

Abstract:With the development of microsurgery method , flap transplantation technology has become increasingly beneficial. To explore the characteristics of the blood supply of flaps, improve the survival rate of flaps, and improve microsurgery technology, many animal models of flaps have been established to simulate the physiological status of flaps in vivo during clinical applications. To date, models of flaps have been established in different animal species with their own advantages and disadvantages. However, there have been no comprehensive summaries of the current state of the field of experimental animal models of flaps. Therefore, we reviewed the current research progress in the field of experimental animal models of skin flaps.