大黄■虫丸联合恩替卡韦抗乙型肝炎性肝纤维化疗效的Meta分析

目的:应用Meta分析评价大黄■虫丸联合恩替卡韦治疗乙型肝炎性肝纤维化的临床疗效、应用价值及研究方向。方法:检索数据库包括知网(CNKI)、万方(WANFANG)、维普(VIP)、中国生物医学数据库(CBM)、PubMed、The Cochrane Library、Embase。检索时间范围系自建库至2022年9月。挑选出大黄■虫丸联合恩替卡韦治疗乙型肝炎肝纤维化的随机对照试验(RCT)，应用RevMan 5.3分析软件分析。结果:文献筛选结果显示，共有8个研究被纳入，包含690例患者，观察组和对照组各有347例和343例。Meta分析结果显示，大黄■虫和恩替卡韦两药联用组对于乙型肝炎性肝纤维化患者血清中透明质酸(HA)、层黏蛋白(LN)、Ⅲ型胶原(PCⅢ)、Ⅳ型胶原(Ⅳ-C)的改善效果优于单用恩替卡韦的对照组，除了Ⅳ型胶原(Ⅳ-C)，其他三项标志物两组间差异均达到统计学显著性。结论:结果显示，大黄■虫丸联合恩替卡韦有良好的抗乙型肝炎性肝纤维化作用，表明大黄■虫丸具有抗乙型肝炎性肝纤维化作用或增强恩替卡韦抗乙型肝炎性肝纤维化作用，提示临床治疗乙型肝炎性肝纤维化时可考虑选用大黄■虫丸和恩...     

Effects of ethanolic extracts of Euonymus alatus on CCl4-induced hepatic fibrosis in mice based on JAK2/STAT3 signaling pathway and its mechanism北大核心CSCD

Aim To explore the mechanism of ethanolic extracts of euonymus alatus on CCl4-induced hepatic fibrosis in mice by regulating JAK2/STAT3 signaling pathway. Methods Sixty C57BL/6J mice were randomly divided into control group,model group,EAL,EAM),EAH,and Silybin(n=10). Except for the control group,mice in other groups were injected with 25% CCl4 of 1.6 mL·kg-1 to induce HF model. Moreover,the positive group was administered 12.6 mg·kg-1 Silybin by gavage once a day,and EAL,EAM,and EAH were administered 72,140 and 280 mg·kg-1 ethanolic extracts of euonymus alatus once by gavage once a day,and the intervention lasted for six weeks. After 6th week,mouse blood was collected,the body weight and liver weight were measured and liver mass index calculated,the liver appearance was observed,and ALT,AST,TNF-α,IL-6,IL-1β were detected in serum. The protein expression levels of collagen Ⅰ,α-SMA,and JAK2/STAT3 signaling pathway-related protein(JAK2,STAT3,p-JAK2,pSTAT3)in mouse liver tissues were detected. Results Compared with the model group,EAM and EAH significantly decreased liver mass index,and the ALT,AST,α-SMA,collagen I levels of serum. After treatment,the liver morphology and structure,cellular inflammatory infiltration,fiber changes and collagen deposition in euonymus alatus intervention group were dose-dependently better than those of the model group. Compared with the model group,the expression of TNF-α,IL-6 and IL-1β in EAM and EAH serum decreased significantly(P<0.05). Compared with the model group,the protein expression levels of JAK2,STAT3,p-JAK2,pSTAT3 in EAM and EAH mouse liver tissues decreased significantly(P<0.05). Conclusion Ethanolic extracts of euonymus alatus have an anti-CCl4-induced HF effect in mice,and its mechanism may be related to the regulation of the JAK2/STAT3 signaling pathway. © 2023 Publication Centre of Anhui Medical University. All rights reserved.     

鬼箭羽醇提取物通过阻止氧化应激和抑制TNF-α-NF-κB及TβR1-Smad2/3通路减轻兔肾缺血再灌注损伤

目的：探讨鬼箭羽乙醇提取物(EEEA)对家兔肾缺血再灌注损伤(RIRI)的作用及其机制。方法：将 30 只家兔随机分成正常组、模型组、低剂量 EEEA(EEEA-L)组、高剂量 EEEA(EEEA-H)组、地塞米松(Dex)组和联合治疗(Dex+EEEA-H)组,每组 5 只。各组动物分别灌胃药物 24 h 后,RIRI 造模,再继续用相应药物灌胃 13 d。其中,正常和模型组家兔灌胃等体积纯水,EEEA-L和 EEEA-H 组家兔分别灌胃 0. 156和 0. 623 g/kg EEEA,Dex组灌胃 0. 2 mg/kg Dex,Dex+EEEA-H 组灌胃 0. 2 mg/kg Dex+0. 623 g/kg EEEA,每天 1 次。分别于第 0、7 和 14 天耳缘静脉采血 2 mL用于检测电解质、肾功能[血尿素氮(BUN)和血清肌酐(SCr)]、超氧化物歧化酶(SOD)、丙二醛(MDA)、白细胞介素 2/6(IL-2/6)、转化生长因子 β₁(TGF-β₁)、肿瘤坏死因子 α(TNF-α)等。第 14 天采血后,以 3% 戊巴比妥钠...     

柔肝降酶方含药血清抑制人肝星状细胞的活化及自噬

背景：自噬在肝纤维化中发挥重要作用,可以通过诱导肝星状细胞活化促进肝纤维化的进程。前期研究表明,柔肝降酶方具有保护肝功能、抗炎、抗氧化应激反应等作用,其是否通过自噬抗肝纤维化的作用机制尚未阐明。目的：探讨柔肝降酶方含药血清对脂多糖诱导的人肝星状细胞活化及自噬的影响及其潜在的作用机制。方法：用脂多糖建立人肝星状细胞活化模型,分成不同的处理组：(1)空白组：人肝星状细胞+空白血清;(2)模型组：人肝星状细胞+空白血清+脂多糖;(3)柔肝降酶方低、中、高剂量含药血清组：人肝星状细胞+低、中、高剂量柔肝降酶方含药血清+脂多糖;(4)柔肝降酶方高剂量含药血清联合雷帕霉素组：高剂量组基础上+雷帕霉素;(5)柔肝降酶方高剂量含药血清联合PI3K抑制剂组：高剂量组基础上+LY294002。CCK-8法观察细胞增殖情况;采用单丹磺酰尸胺染色法观察细胞自噬情况;WesternBlot检测细胞通路蛋白(PI3K、P-PI3K、AKT、P-AKT、mTOR、P-mTOR)、自噬相关蛋白(P62、Beclin-1、LC3-Ⅰ、LC3-Ⅱ)、人肝星状细胞活化标志蛋白(α-平滑肌肌动蛋白、Ⅰ型胶原纤维)表达水平的影...     

大黄素对人类风湿关节炎成纤维样滑膜细胞自噬的影响

目的 基于cGAS/STING信号通路研究大黄素对人类风湿关节炎成纤维样滑膜细胞(MH7A)自噬的潜在作用。方法 采用CCK-8法检测MH7A细胞增殖的结果,并根据细胞存活率筛选出药物的浓度,并加入自噬抑制剂3-MA进一步验证大黄素对自噬的影响;采用MDC法检测MH7A细胞自噬情况;采用蛋白免疫印迹法(Western blot)检测cGAS、STING、p-STING、LC3-I、LC3-II、P62和Beclin-1的蛋白表达水平。结果 MDC染色结果提示,大黄素能够增强MH7A细胞自噬;Western blot结果提示,大黄素可降低MH7A细胞自噬相关蛋白cGAS、STING、p-STING和P62的表达,增加LC3-II和Beclin-1的表达。加入自噬抑制剂3-MA后,MH7A细胞P62蛋白表达升高,LC3-II和Beclin-1蛋白表达降低。结论 大黄素可能通过下调cGAS/STING信号通路加速自噬,抑制MH7A细胞增殖。