OBJECTIVE To investigate and analyze the protective effect of Huayu Jiedu Decoction(HYJD)on the inflammatory injury of cardiomyocytes induced by bacterial lipopolysaccharide(LPS),and its molecular mecha-nism of inhibitory effect on inflammatory response.METHODS H9c2 cells were cultured in vitro and divided into:the blank control group(Control group),the model control group(LPS group),the drug treatment group(HYJD group)and the combined treatment group(LPS+HYJD group).H9c2 cells were treated with different concentrations of HYJD(2.5,5,10,20 and 40 mg/ml)for 24 h,and the activity of H9c2 cells was detected by MTT assay.Additionally,H9c2 cells were treated with LPS-induced myocardial inflammatory injury cell model after 24 h of HYJD intervention at each concentration gradients to detect the cell proliferation changes,as well as to detect the levels of apoptosis of cardiomyocytes and the levels of interleukin(IL)-1β,IL-6,IL-8,IL-10 and tumor necrosis factor(TNF)-α in the culture supernatant of experimental groups,the changes in the protein ex-pression of NO production and the expression changes of iNOS and TLR4/NF-κB signaling pathway protein,and Real-time fluorescence quantitative PCR(qRT-PCR)was used to detect mRNA expression of IL-7R,P38(MAPK)and CXCR2.RESULTS Compared with the Control group,low-concentration HYJD had no significant effect on H9c2 cell viability and did not induce cytotoxic effect,and HYJD increased the survival rate of H9c2 cells in the LPS-induced myocardial inflammatory injury model,and effectively reversed the inhibitory effect of the pro-liferative activity of H9c2 cells induced by LPS.Compared with the control group,the difference in apoptosis level of H9c2 cells in the HYJD monotherapy group was not statistically significant,while the levels of inflammatory apoptosis of H9c2 cells induced by LPS was elevated(P＜0.05).Compared with the LPS group,HYJD inhibited the levels of inflammatory apoptosis in H9c2 cells induced by LPS(P＜0.05),reduced the production of pro-in-flammatory cytokines such as IL-1β,IL-6,IL-8 and TNF-α in the supernatant of the LPS-induced myocardial in-flammatory injury H9c2 cell culture,and upregulated the anti-inflammatory cytokine IL-10.Additionally,com-pared with the Control group,the LPS group showed an increased level of NO release(P＜0.05),while the difference in NO release in the low-concentration(5 mg/ml)HYJD was not statistically significant.Compared with the LPS group,the NO release levels in each HYJD intervention group showed a concentration-dependent de-crease(all P＜0.05).Furthermore,compared with the control group,whereas the expression levels of iNOS and TLR4/NF-κB signaling pathway proteins in the LPS-induced H9c2 cells were both elevated(P＜0.05).CONCLUSION HYJD exhibits protective effects against LPS-induced septic myocardial injury and can exert an in-hibitory effect on inflammatory response,and the molecular mechanisms may be related to the inhibition of the ac-tivation of the TLR4/NF-κB signaling pathway and the down-regulation of the expression of inflammatory genes,etc.,and it may have a good biological activity in the prevention and treatment of septic myocardial injury.

OBJECTIVE To investigate and analyze the protective effect of Huayu Jiedu Decoction(HYJD)on the inflammatory injury of cardiomyocytes induced by bacterial lipopolysaccharide(LPS),and its molecular mecha-nism of inhibitory effect on inflammatory response.METHODS H9c2 cells were cultured in vitro and divided into:the blank control group(Control group),the model control group(LPS group),the drug treatment group(HYJD group)and the combined treatment group(LPS+HYJD group).H9c2 cells were treated with different concentrations of HYJD(2.5,5,10,20 and 40 mg/ml)for 24 h,and the activity of H9c2 cells was detected by MTT assay.Additionally,H9c2 cells were treated with LPS-induced myocardial inflammatory injury cell model after 24 h of HYJD intervention at each concentration gradients to detect the cell proliferation changes,as well as to detect the levels of apoptosis of cardiomyocytes and the levels of interleukin(IL)-1β,IL-6,IL-8,IL-10 and tumor necrosis factor(TNF)-α in the culture supernatant of experimental groups,the changes in the protein ex-pression of NO production and the expression changes of iNOS and TLR4/NF-κB signaling pathway protein,and Real-time fluorescence quantitative PCR(qRT-PCR)was used to detect mRNA expression of IL-7R,P38(MAPK)and CXCR2.RESULTS Compared with the Control group,low-concentration HYJD had no significant effect on H9c2 cell viability and did not induce cytotoxic effect,and HYJD increased the survival rate of H9c2 cells in the LPS-induced myocardial inflammatory injury model,and effectively reversed the inhibitory effect of the pro-liferative activity of H9c2 cells induced by LPS.Compared with the control group,the difference in apoptosis level of H9c2 cells in the HYJD monotherapy group was not statistically significant,while the levels of inflammatory apoptosis of H9c2 cells induced by LPS was elevated(P＜0.05).Compared with the LPS group,HYJD inhibited the levels of inflammatory apoptosis in H9c2 cells induced by LPS(P＜0.05),reduced the production of pro-in-flammatory cytokines such as IL-1β,IL-6,IL-8 and TNF-α in the supernatant of the LPS-induced myocardial in-flammatory injury H9c2 cell culture,and upregulated the anti-inflammatory cytokine IL-10.Additionally,com-pared with the Control group,the LPS group showed an increased level of NO release(P＜0.05),while the difference in NO release in the low-concentration(5 mg/ml)HYJD was not statistically significant.Compared with the LPS group,the NO release levels in each HYJD intervention group showed a concentration-dependent de-crease(all P＜0.05).Furthermore,compared with the control group,whereas the expression levels of iNOS and TLR4/NF-κB signaling pathway proteins in the LPS-induced H9c2 cells were both elevated(P＜0.05).CONCLUSION HYJD exhibits protective effects against LPS-induced septic myocardial injury and can exert an in-hibitory effect on inflammatory response,and the molecular mechanisms may be related to the inhibition of the ac-tivation of the TLR4/NF-κB signaling pathway and the down-regulation of the expression of inflammatory genes,etc.,and it may have a good biological activity in the prevention and treatment of septic myocardial injury.

Objective To investigate the effect of tetrahydrobiopterin (BH₄), superoxide dismutase-polyethylene glycol (PEG-SOD) and N(G)-nitro-L-arginine (L-NNA) on impaired endothelial progenitor cell (EPC) functions in DOCA-salt hypertensive mice. Methods DOCA-salt hypertension was created and systolic blood pressure was measured by tail-cuff methods. EPC was isolated from bone marrow of mice and characterized by flow cytometry and fluorescence microscopy. EPC of DOCA-salt mice was incubated with BH₄, PEG-SOD, and L-NNA for 24 h, then in vitro EPC function assays were performed. Results Compared with control group, systolic blood pressure was significantly increased in DOCA-salt mice. Both EPC adhesion and angiogenesis functions were impaired in DOCA-salt mice compared to control animals, which were reversed by incubation with BH₄, PEG-SOD and L-NNA. Conclusion BH₄, PEG-SOD and L-NNA rescued the impairments from EPC functions in DOCA-salt hypertensive mice.

Objective: To explore the improvement rate of liver fibrosis in patients with chronic hepatitis B virus infection who received entecavir alone or in combination with anluohuaxianwan for 78 weeks. Methods: Patients with chronic HBV infection were randomly treated with entecavir alone or in combination with anluohuaxian for 78 weeks. Ishak fibrosis score was used for blind interpretation of liver biopsy specimens. The improvement in liver fibrosis condition before and after the treatment was compared. Student's t test and non-parametric test (Mann-Whitney U-Test and Kruskal-Wallis test) were used to analyze the measurement data. The categorical variables were analyzed by Chi-square test method and Spearman’s rank correlation coefficient was used to test bivariate associations. Results: Liver fibrosis improvement rate after 78 weeks of treatment was 36.53% (80/219) and the progression rate was 23.29% (51/219). The improvement of liver fibrosis was associated to the degree of baseline fibrosis and treatment methods (P < 0.05). The improvement rate of hepatic fibrosis in patients treated with anluohuaxianwan combined with entecavir at baseline F < 3 (54.74%, 52/95) was significantly higher than that in patients treated only with entecavir (33.33%, 16/48), P = 0.016 and the progression rate of hepatic fibrosis (13.68%, 13/95) was lower than that in patients treated alone (18.75%, 9/48), P = 0.466. In patients with baseline F < 3, the proportion of patients with improved and stable liver fibrosis in the combined treatment group (68.1%, 32/47) was higher than that in the treatment group alone (51.7%, 15/29). Conclusion Combined anluohuaxianwan and entecavir treatment can significantly improve the improvement rate of liver fibrosis in patients with chronic hepatitis B virus infection. Furthermore, it has the tendency to improve the stability rate and reduce the rate of progression of liver fibrosis.

Subjective memory decline is one of the most common symptoms reported in the elderly,which is considered as a high-risk factor for dementia.This article presented an overview of an update of definition and epidemiology of subjective memory decline,reviewed its risk factors,and summarized neuroimaging changes in brain structure and function.Finally,some suggestions for future research were also proposed.

Objective:The present study was designed to test the hypothesis that inflammation is involved in the end-organ damage(EOD) induced by sinoaortic denervation(SAD) in rats.Method:SAD was performed in male Sprague-Dawley rats at the age of 10 weeks.Under anaesthesia,aortic nerves were cut and the sinus region of the carotid artery was stripped and painted with 10% phenol.Pathological evaluation of EOD and the determination of plasma or tissue levels of the factors related to inflammation,including thromboxane B2(TXB2) interleukin-1(IL-1),tumour necrosis factor α(TNF-α) and reactive oxygen species(ROS) were performed at 16 weeks after SAD.Pathological evaluation of EOD included heart weigh ratio,myocardial and blood vessel hydroxyproline and collagen volume fraction,glomerular injury score and number of infiltrating inflammatory cells.Indomethacin(20 mg/kg per day,orally) or vitamin E(100 mg/kg per day,orally) was administered for 12 weeks,beginning from4 weeks after SAD,to observe their effects on SAD-induced EOD.Results:There were significant fibrosis and inflammatory infiltration in the myocardium and blood vessels,represented by higher hydroxyproline and collagen volume fraction,and a large amount of inflammatory cells in the tissues of SAD rats.Heart weight and kidney glomerular injury score were significantly higher in ed significantly after SAD.Indomethacin and vitamin E significantly decreased the contents of some factors related to inflammation in SAD rats.Both drugs also alleviated myocardial and vessel fibrosis,inflammatory infiltration and kidney damage.Conclusion:Inflammation is involved in the organ damage induced by SAD in rats.