Mechanism of Fufang Congrong Yizhi Capsules in treatment of mild cognitive impairment based on network pharmacology / 中国药理学通报

Aim To predict the mechanism of Fufang Congrong Yizhi Capsules (FCYC) in the treatment of mild cognitive impairment (MCI) by network pharmacology method, and further validate it in combination with cellular experiments. Methods TCMSP, Gene-Cards, OMIM and TTD databases, Chinese Pharmacopoeia and related literature were used to screen the active ingredients of FCYC and the targets of MCI treatment. The TCM-compound-target-disease network and PPI of intersection targets were constructed, and the GO and KEGG analysis were performed by the Ehamb bioinformation platform. GO and KEGG analysis were performed through Yihanbo biological information platform. Cell model of MCI was established by PC-12 injury induced by Aβ

Effect of SMAC Gene on Sensitivity of Lung Adenocarcinoma Cells to Paclitaxel and Cell Viability Based on caspase-3/Bcl-2/Bax Signaling Pathway / 肿瘤防治研究

Objective To investigate the effect of the SMAC gene on paclitaxel sensitivity and cellular activity in lung adenocarcinoma cells based on the caspase-3/Bcl-2/Bax signaling pathway. Methods A paclitaxel-resistant cell line A549/Taxol was established for lung adenocarcinoma, and the cells were divided into four following groups: pcDNA-NC (transfected with pcDNA-NC blank vector), pcDNA-SMAC (transfected with pcDNA-SMAC vector), siRNA-NC (transfected with siRNA-NC empty virus vector), and siRNA-SMAC groups (transfected with siRNA-SMAC lentiviral vector). The SMAC mRNA expression in cells was detected by qRT-PCR; cell sensitivity was detected by MTT; cell proliferation ability was detected by cloning assay; cell invasion ability was detected by Transwell; apoptosis ability was detected by flow cytometry assay; and caspase-3, Bcl-2 and Bax protein expression in cells were detected by Western blot analysis. Results The SMAC mRNA expression was significantly lower in A549 cells compared with BEAS-2B cells (P < 0.05). The SMAC mRNA expression was significantly higher in the pcDNA-SMAC group than that in the pcDNA-NC group cells (P < 0.05). The SMAC mRNA expression was significantly lower in the cells of the siRNA-SMAC group (P < 0.05) than that in the siRNA-NC group. The SMAC mRNA expression was significantly lower in the cells of the siRNA-SMAC group (P < 0.05) than in the siRNA-NC group. Compared with the pcDNA-NC group, the cell IC50, cell clone number, cell invasion ability, and Bcl-2 protein and Bcl-2/Bax ratio were significantly lower in the pcDNA-SMAC group, the cell resistance index reversal was 2.51-fold, and the apoptosis ability and caspase-3, as well as Bax protein expression, were significantly higher (P < 0.05). Compared with the siRNA-NC group, cell IC50, cell clone number, cell invasion ability, and Bcl-2 protein and Bcl-2/Bax ratio were significantly higher in the siRNA-SMAC group, and apoptosis ability and caspase-3 and Bax protein expression were significantly lower (P < 0.05). Conclusion High expression of SMAC increases paclitaxel sensitivity, inhibits cell growth and invasion, promotes apoptosis in lung adenocarcinoma cells, and has a regulatory effect on the caspase-3/Bcl-2/Bax signaling pathway.

The protective effect of trigonelline on H / 中国药理学通报

Aim To study the protective effect of trigonelline on H

CircRNA-32011 regulates apoptosis induced by arsenic trioxide in cardiac myocytes / 中国药理学通报

Aim To investigate the effect of circRNA- 32011 on myocardial apoptosis induced by arsenic triox- ide (ATO).Methods Primary cardioniyocytes of suckling neonate mouse were treated with ATO ( final concentration 10 (xniol • L_1 ) for 24 h.Then cell via¬bility was measured by M IT assay.The mKNA expres¬sion levels of Bel-2/ Bax and circRNA-3201 I were de¬tected by KT-PCK.Bcl-2/Bax protein expression lev¬els were detected by Western blot.Overexpression and knock down circHNA-32011 respectively by plasmid and siHNA were used to verify its function in ATO-in- duced cardiomyocyte apoptosis.Results Myocardial cell viability decreased, Bel-2 expression significantly decreased while Bax expression increased in ATO group compared with the control group.CircKNA- 32011 was down-regulated in ATO ineuhated cardio¬niyocytes.Ovcrex press ion of circRNA-32011 in ATO- incubated cardioniyocytes increased myocardial cell vi¬ability and Bel-2 expression and decreased the expres¬sion of Bax.Knockdown of circRNA-32011 could fur¬ther reduce cardiomyoevte activity and Bel-2 expression and increase the experssion of Bax induced by ATO.Conclusions CircRNA-32011 protects cardiac myo¬cytes from apoptosis induced by arsenic trioxide, which may provide a new potential therapeutic strategy for ATO-induced myocardial injury.

The protective effect of nerve function of Buyang Huanwu decoction on cerebral ischemia/reperfusion rats after neural stem cell transplantation / 中国药理学通报

To explore the protective effect of nerve function of Buyang Huanwu Decoction on cerebral ischemia/reperfusion rats after the transplantation of neural stem cells (NSCs) . Methods Thread bolt method was used to establish middle cerebral artery occlusion model. Drug groups were given Buyang Huanwu Decoction (14. 8 g kg"1 d " 1) by gavage after the rats being sober. NSCs were transplanted to rat brain after making the model 24 hours later. Zea Longa neurobehavioral behavioral score was used to observe neural function defect, and TTC staining to detect the volume of cerebral infarction, and Nissl staining to detect Nissl body integrated optical density (IOD), and Immunohistochemical staining to detect expression of Bcl-2 and Bax. Results Compared with sham operation group, the nerve function defect appeared, and the volume of cerebral infarction increased significantly, the integral optical density of Nissl body was reduced and the ratio of Bcl-2 to Bax was reduced in model group (P < 0. 05) . Compared with model group, the nerve function defect was reduced, the volume of cerebral infarction was reduced, the integral optical density of Nissl body increased, and the ratio of Bcl-2 to Bax increased in BYHWD group, Transplant group and BYHWD + Transplant group (P < 0. 05). Compared with transplant group, the nerve function defect was reduced, the volume of cerebral infarction was reduced , the integrated optical density of Nissl body increased , and the ratio of Bcl-2 to Bax increased in BYHWD + Transplant group (P < 0. 05). Conclusions Buyang Huanwu Decoction can enhance the neuroprotective effect after NSCs transplantation in cerebral ischemia/reperfusion rats.

Study on the effect and mechanism of hepatitis B virus X protein transactivates gene 4 in HepG2 cell apoptosis / 中华肝脏病杂志

Objective@#To investigate the effect and mechanism of XTP4 gene in apoptotic hepatoblastoma HepG2 cell line.@*Methods@#HepG2 cells were transiently transfected with small interfering RNA of XTP4 genes, plasmid pcDNA3.1/myc-His(-) A-XTP4, and hepatitis B virus X protein transactivated x gene 4 (HBX protein trans-activate gene4, XTP4) and their respective negative controls. After 48h, the overexpression and interference expression condition of XTP4 in HepG2 cells were detected by Western blot. HepG2 cells apoptosis was detected by flow cytometry. The expression levels of apoptosis-related proteins P53, Bcl-2, Bax and Caspase-3 in HepG2 cells were detected by Western blot, and Bcl-2/Bax ratio was calculated. The chemiluminescence assay was used to detect activity of caspase-3 in HepG2 cells. The measured data were presented as ( ± s), and independent sample t-test was used for comparison between the two groups.@*Results@#HepG2 cells had successfully achieved the overexpression and interference expression of XTP4 protein. Compared with the control group, the overexpression of XTP4 in HepG2 cells had significantly decreased the number of apoptotic cells (P < 0.05), and increased Bcl-2/Bax (P < 0.05) ratio, but decreased the expression of P53 protein (P < 0.05). The protein expression of Caspase-3 and activity of caspase-3 was decreased (P < 0.05). However, interference with XTP4 expression in HepG2 cells had significantly increased the number of apoptotic cells (P < 0.05) and decreased Bcl-2/Bax (P < 0.05) ratio, but increased the expression of P53 protein (P < 0.05). The protein expression of Caspase-3 and activity of caspase-3 was increased (P<0.05).@*Conclusion@#In HepG2 apoptosis XTP4 has inhibitory effect, and its effect on inhibiting HepG2 apoptosis may be achieved by regulating the Bcl-2/Bax ratio, and the P53 protein may be involved.

Effect of fracture of lower limbs with hemorrhage on myocardial injury and its mechanism in rats / 中国应用生理学杂志

OBJECTIVES@#To test whether myocardial apoptosis can be induced by traumatic fracture of lower limbs with hemorrhage, in order to lay a foundation of myocardial injury after traumatic fracture for the follow-up study.@*METHODS@#Twenty SD rats were randomly divided into two groups, i. e. control group and trauma group(=10). A rat model of traumatic hemorrhage was establish, and a traumatic model of the original generation of myocardial cell culture was constructed . The level of interleukin-2(IL-2),IL-6,IL-10 and tumor necrosis factor-α(TNF-α) in rat serum was detected by ELISA at 0, 1, 2, 4, 8, 12, 16, 24 and 48 hour to find the most significant point. The pathological cardiac injury in rats was observed by HE staining under a microscope, and the apoptosis of cultured cardiomyocyte was detected by TUNEL methods. The expressions of apoptosis gene,(Bcl-2) and Bax, in myocardium of rat and cultured cardiomyocyte were detected by Western blot and RT-PCR.@*RESULTS@#At the 4 hour after trauma, IL-6 and IL-10 in the serum of rats reached its highest, IL-2 reached its lowest at the 8th hour after trauma, and TNF-αreached its highest at 1 hour after trauma, then all recovered to their normol level gradually. Myocardial HE staining indicated that cardiomyocyte was swelling, disordered derangement, inflammatory cell infiltrated; a large number of myocardial cell nuclei was dyedbrown in TUNEL test which proved that the apoptosis index increased (<0.05). Western blot and RT-PCR results showed that the expression of pro-apoptotic gene Bax was up-regulated (<0. 05), while expression of anti apoptosis gene Bcl-2 down-regulated (<0.05).@*CONCLUSIONS@#The myocardial apoptosis can be induced by traumatic fracture of lower limbs with hemorrhage in rats, and then lead to myocardial injury.

Effects of rice peptide YGEGSSEEG on improving endothelial cell injury induced by tumor necrosis factor / 中国药理学通报

Aim To investigate the peptides and its protection for vascular endothelial cells, derived from the absorbed components of rice α-globulin,which was shown to be effective in anti-atherosclerosis. Methods The amino acid sequence was purified by gel chro-matography and RP-HPLC, and determined by ESI/MS. Then the peptide was chemically synthesized. Hu-man umbilical vein endothelial cell injury model was induced by tumor necrosis factor-α. The cell viability was measured by cell counting kit to screen the appro-priate peptide intervention concentration. The apoptotic rate was detected by flow cytometry. Bcl-2, Bax, p-p38, vascular cell adhesion molecule and the protein expression level of NF-κB signaling pathway were de-tected by Western blot and immunofluorescent stai-ning. Results Apoptosis of HUVECs induced by TNF-α was significantly increased by YGEGSSEEG, which also regulated expression of Bcl-2/Bax proteins and inhibited phosphorylation of p38 protein. Besides, the peptide suppressed the production of VCAM-1, ICAM-1 and activation of NF-κB pathway. While it did not significantly improve the oxidative stress response in HUVECs. Conclusion Peptide YGEGSSEEG pro-tects vascular endothelial cells through suppressing ap-optosis and expression of adhesion molecules.

Allicin improves cardiac function by protecting against apoptosis in rat model of myocardial infarction / 中国结合医学杂志

<p><b>OBJECTIVE</b>To study the effects of allicin on cardiac function and underlying mechanism in rat model of myocardial infarction (MI).</p><p><b>METHODS</b>Ninety-four Wistar rats were randomly assigned to 6 groups (n=14-16 per group): sham control group [underwent thoracotomy without left anterior descending (LAD) occlusion and only received an injection of the same amount of citrate buffer], MI control group (subjected to LAD occlusion and only received an injection of same amount of citrate buffer), positive control group (subjected to LAD occlusion and received an injection of diltiazem hydrochloride at the dose of 1.5 mg/kg), and MI + allicin groups (subjected to LAD occlusion and received an injection of allicin at the doses of 1.2, 1.8, and 3.6 mg/kg). All of the drugs were administered intraperitoneally daily for 21 days. The infarct area was measured by myocardial staining. Hematoxylin-eosin staining was used to observe the pathological changes. Cardiac function parameters were assessed by echocardiography. The myocardial apoptotic index was estimated by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling staining. The expression of Bax and Bcl-2 were detected by quantificational real-time polymerase chain reaction and Western blot.</p><p><b>RESULTS</b>Treatment with allicin could attenuate the myocardial infarct area (P<0.05) and relieve the changes of the myocardium. The left ventricular anterior wall diastolic and systolic thicknesses were increased in the allicin-treated groups (P<0.05), while there was no signifificant difference in the left ventricular posterior wall diastolic and systolic thickness (P>0.05). The left ventricular internal diameter in systole, ejection fraction, fractional shortening, and stroke volume were dramatically elevated in allicin-treated rats (P<0.05). Allicin dose-dependently reduced creatine kinase and lactate dehydrogenase levels (P<0.05). The myocardial apoptotic index was also markedly lowered, and Bax expression was signifificantly decreased, whereas Bcl-2 expression exhibited an opposite trend in allicin-treated rats (P<0.05).</p><p><b>CONCLUSION</b>Allicin appears to exert a cardioprotective effect that may be linked to blocking Bcl-2/Bax signaling pathway-denpendent apoptosis, further improving cardiac function.</p>

Effect of nourishing kidney,activating blood and expelling toxin method Chinese medicine on renal cells apoptosis in CKD rats / 重庆医学

Objective To observe the curative effect of nourishing kidney,activating blood and expelling toxin method Chinese medicine on chronic kidney disease (CKD) ratsand influence on cellular apoptosis.Methods The UUO animal model was adopted.SD male rats were divided into the sham operation group,UUO model group,Chinese medicine low dose group and high dose group.The renal function was measured by the automatic biochemical analyzer,the renal histopathologic change was observed by HE staining,the renal tissue apoptosis rate was observed by TUNEL as well as the protein expression levels of Bcl-2 and Bax were detected by Western blot.Results Compared with the UUO model group,the levels of serum creatinine(Scr) and urea nitrogen(BUN) in Chinese medicine various doses groups were significantly decreased(P＜0.05).In the UUO pathologic observation,renal tubular epithelial cells apoptosis,necrosis,exfoliation,inflammatory cells infiltration were found in the model group,the renal damage in the Chinese medicine various doses groups were slighter compared with the UUO group(P＜0.05).The TUNEL method detection showed that the cellular apoptosis number in the UUO group was significantly increased compared with the sham operation group,the Chinese medicine various doses groups could significantly decrease the apoptosis number(P＜0.05).Compared with the UUO model group,the level of Bcl-2 in the Chinese medicine treatment groups was markedly up-regulated,the Bax level was down-regulated,and the ratio of Bcl-2/Bax was increased(P＜0.05).Above results all showed the dose dependent manner.Conclusion The nourishing kidney,activating blood and expelling toxin method Chinese medicine can obviously down-regulate serum Scr and BUN levels,inhibits the renal cells apoptosis in UUO rat and regulates the Bcl-2 and Bax levels.