Background: Gastric cancer (GC) is marked by high incidence, malignancy, and poor prognosis. Understanding its development mechanisms and discovering effective drugs are urgent needs. Elevated oxidative stress levels in GC patients have been linked to disease progression. Berberine, an isoquinoline alkaloid from Coptis chinensis, exhibits strong anti-GC properties without notable side effects. However, its impact and mechanisms regarding oxidative stress in GC remain unclear. This study aims to explore berberine's anti-GC mechanisms through network pharmacology and validate findings via in vitro experiments. Methods: Berberine's target genes were sourced from the Traditional Chinese Medicine Systems Pharmacology (TCMSP) and Comparative Toxicogenomics Database (CTD). GC-related targets were gathered from GeneCards, Online Mendelian Inheritance in Man (OMIM), PharmGkb, the Therapeutic Target Database (TTD), and DrugBank. The intersection of these targets facilitated the construction of a "drug-disease-target" network using Cytoscape 3.9.1. A protein-protein interaction (PPI) network was developed via the STRING database, and core targets were identified through visualization and topological analysis. Gene Ontology (GO) functional and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed using R. Subsequently, in vitro experiments validated the pharmacology predictions, evaluating berberine's effects on AGS and MKN45 GC cell viability and migration through Cell Counting Kit-8 (CCK-8) and cell scratch assays. The impact of berberine on reactive oxygen species (ROS), malondialdehyde (MDA), and superoxide dismutase (SOD) levels was assessed using specific detection kits. Additionally, the influence of berberine on oxidative stress-related signaling pathways nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1), hypoxia-inducible factor-1 alpha (HIF-1 alpha), and epithelial-mesenchymal transition (EMT) was assessed through Western blot analysis. Results: Network pharmacology analysis identified 281 targets for berberine and 8,953 targets related to GC, revealing 224 common targets. GO enrichment analysis encompassed 3,001 biological processes, with the top 10 including responses to external biotic stimuli, oxidative stress, nutrient levels, chemical stress, oxygen levels, and hypoxia. Additionally, 122 cellular components and 213 molecular functions were identified. KEGG pathway enrichment analysis indicated 176 related signaling pathways, with key pathways for berberine's anti-GC effects potentially including phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT), forkhead box O (FOXO), and HIF-1. In vitro experiments demonstrated that berberine significantly inhibited GC cell activity and migration, increased intracellular levels of ROS and MDA, reduced levels of SOD, and suppressed the expression of Nrf2/HO-1, HIF-1 alpha, and EMT pathway proteins. Conclusions: Regulation of oxidative stress may be one of the key mechanisms by which berberine inhibits the progression of gastric cancer.

目的 探讨黄芪甲苷对氯吡格雷致大鼠胃黏膜损伤的治疗作用及机制.方法 将50只SD大鼠随机分为对照组、模型组及黄芪甲苷低、中、高剂量组,每组10只,分别予生理盐水1 mL/100 g、氯吡格雷15.6 mg/kg、氯吡格雷15.6 mg/kg+黄芪甲苷15、30、60 mg/kg灌胃,每日1次,干预1周后脱颈处死大鼠.用损伤指数评分评价胃黏膜损伤情况,用免疫组化SABC染色法检测胃黏膜组织中血管内皮细胞生长因子(VEGF)、磷酸化血管内皮细胞生长因子受体2(p-VEGFR2)蛋白表达.结果 与对照组比较,模型组胃黏膜损伤指数评分高,VEGF、p-VEGFR2蛋白表达低(P均<0.05);与模型组比较,各黄芪甲苷组胃黏膜损伤指数评分均低,VEGF、p-VEGFR2蛋白表达高(P均<0.05);黄芪甲苷低、中、高剂量组胃黏膜损伤指数评分逐渐降低,VEGF、p-VEGFR2蛋白表达逐渐升高(P均<0.05).结论 黄芪甲苷可减轻氯吡格雷所致胃黏膜损伤,其作用机制可能与上调VEGF、p-VEGFR2表达有关.

目的 观察复方聚乙二醇(PEG)电解质散联合利那洛肽行肠道准备,在结肠镜检查中的效果和安全性.方法 选取2022年3月1日-2022年8月30日该院收治的拟进行结肠镜检查的75例患者作为研究对象,采用随机数表法,将75例患者随机分为观察组、对照组A和对照组B,每组各25例.对照组A单用2 L复方PEG电解质散行肠道准备,对照组B单用3 L 复方PEG电解质散行肠道准备,观察组采用利那洛肽联合2 L复方PEG电解质散行肠道准备.使用波士顿肠道准备评估量表(BBPS)评估患者肠道清洁度情况,统计患者满意度、不良反应发生率和肠道息肉检出率.结果 观察组的肠道准备效果优于对照组A,息肉检出率高于对照组A;观察组患者满意率高于对照组B,不良反应总发生率低于对照组B,差异均有统计学意义(P<0.05).结论 利那洛肽联合2 L复方PEG电解质散的方案,可提高BBPS、息肉检出率和患者满意度,降低肠道准备过程中不良反应发生率,值得临床应用.

Objective:To systematically evaluate the efficacy and safety of tissue adhesive combined with lauromacrogol (modified Sandwich method) for gastric varices.Methods:Literature in the Cochrane Library, PubMed, EMbase, CNKI, VIP and Wanfang were searched by two independent researchers from the establishment of the databases to June 30, 2020, and qualified data from the eligible literature were extracted. Revman 5.3 was used to analyze outcomes including hemostatic efficiency, incidence of postoperative fever, chest and abdominal pain, ulcer, ectopic embolism and complications, and postoperative re-bleeding rate (Mantel-Haenszel method).Results:A total of 8 randomized controlled trials including 898 patients were included in this meta-analysis. The results showed that compared with the classic Sandwich method, the modified version had a better hemostatic effect ( P=0.01, OR=2.07, 95% CI: 1.17-3.68) and a lower incidence of postoperative ectopic embolism ( P=0.001, OR=0.06, 95% CI: 0.01-0.34). There were no significant differences in the incidences of postoperative fever ( P=0.58, OR=0.86, 95% CI: 0.52-1.44), chest and abdominal pain ( P=0.83, OR=0.95, 95% CI: 0.58-1.56), local ulcer ( P=0.31, OR=0.66, 95% CI: 0.30-1.47) , re-bleeding ( P=0.14, OR=0.76, 95% CI: 0.53-1.09) or overall incidence of adverse reactions ( P=0.24, OR=0.66, 95% CI: 0.33-1.32). Conclusion:The modified Sandwich method of tissue adhesive combined with lauromacrogol is an effective and safe method in the treatment of gastric varices.

代谢相关脂肪性肝病(MAFLD)是人类健康的一大威胁,研究MAFLD具有重要的现实意义.目前认为,MAFLD的发病与脂质代谢障碍、氧化应激、炎症反应和胰岛素抵抗等因素有关;肠道菌群作为近年来的研究热点,同样参与了MAFLD的多个发病环节.过氧化物酶体增殖物激活受体(PPAR)是机体内脂质代谢和糖代谢的关键性调节因素,参与MAFLD的发病,而肠道菌群和PPAR之间亦相互作用.现就肠道菌群-PPAR信号通路在MAFLD发病中的作用研究进展进行综述.

Objective : Astragaloside IV (AS-IV) is the primary bioactive component purified from Astragalus membranaceus which is one of the traditional Chinese medicines. Research studies found that AS-IV has significant pharmacological effects on focal cerebral ischemia/reperfusion, cardiovascular disease, pulmonary disease, liver cirrhosis, and diabetic nephropathy, but little is known about the effects of AS-IV on nonalcoholic fatty liver disease (NAFLD). In this study, we investigated whether AS-IV has beneficial effects on NAFLD in rats and its potential mechanisms. Methods : Male SD rats were fed with high-fat diet (HFD) for 12 weeks to establish NAFLD rat model, and then, the rats were divided into five groups. The control group rats were fed with normal diet for 12 weeks and then were given normal saline (1.0 ml kg −1 day −1 ) by intragastric administration for 4 weeks. The model group rats were fed with HFD for 12 weeks and then were given normal saline (1.0 ml kg −1 day −1 ) by intragastric administration for 4 weeks. The AS-IV-L, AS-IV-M, and AS-IV-H groups were treated with 20, 40, and 80 mg kg −1 day −1 of AS-IV by intragastric administration for 4 weeks and given HFD diet. Then, we detected serum transaminase (ALT, AST), blood lipid (TG, TC), inflammatory cytokines (IL-6, IL-8 and TNF-α), liver histology(NAFLD activity score), TLR4/MyD88 signaling pathway in liver tissue. Results : We found AS-IV significantly reduced serum levels of AST, ALT, TG, TNF-α, IL-6, and IL-8 in NAFLD rats and downregulate the expression of TLR4 mRNA, MyD88 mRNA, NF-κB mRNA, and proteins in liver tissue. Moreover, AS-IV could significantly reduce the NAFLD activity score of NAFLD rat liver. Conclusion : In this study, we demonstrated that AS-IV have a protective effect on NAFLD by inhibiting TNF-α, IL-6 and IL-8 levels and down-regulating TLR4, MyD88 and NF-κB expression in rat liver tissues.

患者为老年男性，既往有2型糖尿病、冠状动脉粥样硬化性心脏病、高血压、便秘等慢性疾病。主因腹胀、上腹部不适3个月，加重伴腹痛3 d入院。3个月前经结肠镜检查确诊为结肠黑变病，未行治疗。入院后腹部CT检查提示结肠气囊肿综合征，予甲硝唑、枯草杆菌二联活菌肠溶胶囊口服，同时予高压氧治疗，5 d后腹痛消失，10 d后复查腹部CT示原结肠周围多发气体和部分肠壁气体密度影消失。结肠气囊肿是一种预后良好的少见疾病，结肠黑变病合并结肠气囊肿临床罕见。结肠黑变病可引起肠道蠕动减少、肠壁菲薄、肠道压力升高，可能是结肠气囊肿的诱因之一。

目的 探讨黄芪甲苷对氯吡格雷所致大鼠胃黏膜损伤的保护作用及血清IL-6、IL-8、TNF-α的影响.方法 健康雄性SD大鼠50只,随机分为对照组、模型组及黄芪甲苷低、中、高剂量组,每组10只,分别予生理盐水、氯吡格雷、氯吡格雷联合不同浓度黄芪甲苷灌胃,每日1次,7d后处死大鼠.Guth法测定胃黏膜溃疡指数;ELISA法检测血清IL6、IL-8、TNF α水平;光镜下观察大鼠黏膜病理形态变化.结果 与对照组相比,模型组大鼠胃黏膜损伤指数升高,差异有统计学意义(P＜0.01);与模型组相比,各实验组大鼠胃黏膜损伤指数改善,差异有统计学意义(P＜0.05);模型组血清IL6、IL-8、TNF α水平明显高于对照组,差异有统计学意义(P＜0.05);与模型组相比,各实验组血清IL6、IL-8、TNFα水平降低,差异有统计学意义(P＜0.05).结论 黄芪甲苷可以通过降低血清炎性因子IL-6、IL-8、TNF-α水平对氯吡格雷所致胃黏膜损伤发挥保护作用.

Background:Irritable bowel syndrome(IBS)is a commonly seen functional gastrointestinal disorders(FGIDs),and can reduce the quality of life and has some effects on patients'psychology. Aims:To investigate the disorder of sleep and psychological status in patients with IBS and IBS overlapping other FGIDs,and to analyze their risk factors. Methods:Questionnaires were conducted among FGIDs patients from January 2014 to December 2014 in 6 hospitals at Tianjin. Pittsburgh sleep quality index(PSQI)was used to assess sleep quality,anxiety and depression were assessed by self-rating anxiety scale(SAS)and self-rating depression scale(SDS),respectively. Two-factor Logistic regression analysis was used to analyze the risk factors of sleep disorder in patients with IBS overlapping other FGIDs. Results:A total of 1 117 patients with FGIDs completed the questionnaires,including 32 IBS patients(2. 9%)and 113 patients(10. 1%)with IBS overlapping other FGIDs. The percentages of sleep disorder,psychological disorder,and combination of the two were 59.4%,93.8% and 59.4% in IBS group,respectively;and 82.3%,95.6% and 78.8% in IBS overlapping other FGIDs group,respectively. Gender,age and severity of symptoms were the risk factors of sleep disorder in patients with IBS overlapping other FGIDs(P=0.014,P=0.049,P=0.025). Conclusions:Both IBS patients and IBS overlapping other FGIDs patients are associated with varying degrees of sleep disorder and/or psychological disorder. Gender,age and severity of symptoms may be the risk factors of sleep disorder in IBS overlapping other FGIDs patients.

Background. Functional gastrointestinal disorder (FGID) patients are influenced by anxiety, depression, and low sleep quality, which reduce the quality of their life. However, epidemiological data on the quality of sleep in FGID patients were lacking. This study aims to explore the sleep quality and influencing factors of the sleep quality in FGID patients. Methods. 1200 subjects, diagnosed as FGID in one of the six class-three hospitals in Tianjin, China, from January to December 2014, were recruited. The information about demographic information, the severity of clinical symptoms, psychological status (Zung self-rating depression scale), and sleep quality (evaluated with Pittsburgh sleep quality index) was gathered. Results. The questionnaires from 1117 participants were collected including 920 of functional dyspepsia (FD) patients, 77 of irritable bowel disease (IBS) patients, 26 of functional constipation (FC) patients, and 94 other FGID patients. The results showed that morbidity rate for FD patients who had sleep disorders was higher than those who suffered from IBS or FC (P<0.001). The proportion of elderly patients suffering from low sleep quality was higher than that of middle-aged and young patients (P<0.001). The binary logistic regression analysis showed that age, education, and the severity of FGID symptom were influencing factors for poor sleep quality in FGID patients. Conclusion. The issue of poor sleep quality in FGID patients in Tianjin area is prominent, and elderly patients suffer lower sleep quality than other FGID patients. Age, education, and the severity of FGID symptoms are critical influencing factors which result in a drop-in sleep quality.

Objective To analyze the status of sleep disorders in patients with functional gastrointestinal disease （FGID）and its relation with symptom characteristics. Methods From January to December 2014,questionnaire was carried out in FGID patients who met the Rome Ⅲ criteria

Non-alcoholic fatty liver disease is a metabolic stress disorder which is closely related to insulin resistance and genetic susceptibility. As the living standards continue improving, the prevalence has been rising. Non-alcoholic fatty liver disease can not only cause seriously abnormal liver transaminases, decompensated cirrhosis, liver failure and so on, but also is associated with cardiovascular disease, type 2 diabetes and metabolic syndrome, which is a serious threat to the health of people. Therefore, the treatment of non-alcoholic fatty liver disease causes more and more attention, and the treatment principles include:①Removal of the cause and to treat the primary underlying diseases;②Basic measures of treatment:lifestyle intervention, dietary modification, exercise therapy and so on; ③To give a supplementary drug therapy varying from person to person according to different pathologic features; ④For end-stage liver disease, liver transplantation is recommend. This article will focus on lifestyle interventions, weight loss surgery and drug treatment progress.

目的 研究双联抗血小板治疗相关上消化道出血(UGIB)的临床特点.方法 收集双联抗血小板治疗相关UGIB 住院患者59例为观察组,随机选取同期非抗血小板治疗的UGIB 患者120例作为对照组,对两组患者的临床资料进行比较.结果 两组患者在性别、贫血程度、幽门螺杆菌感染等方面无显著差异(P>0.05).但是观察组患者的年龄较对照组高(P=0.000),观察组出血之前缺乏典型腹痛症状者明显增多(P=0.000),出血症状中缺乏呕血和黑便症状,仅以乏力贫血就诊者明显增多(P=0.001).观察组内镜表现为黏膜糜烂患者增多,但无统计学差异(P=0.269).观察组患者均合并冠心病,57.63%合并急性冠脉综合征,与对照组有显著差异(均P=0.000).观察组住院时间明显延长(P=0.000),病死率明显增高(P=0.023).结论 应加强对双联抗血小板治疗相关UGIB 临床特点的认识,减少抗血小板药物不良反应.

The present study aimed to investigate the impacts of telmisartan (TEL) on hepatic fibrosis, serum leptin, leptin protein in liver tissue and its mRNA expression level in rats with non-alcoholic fatty liver disease (NAFLD). Male Sprague Dawley rats were randomly divided into the control (N), model (M), polyene phosphatidylcholine (P) and TEL (T) groups. Group M and the intervention groups were given a high-fat diet for 12 weeks to induce NAFLD, followed by 4 weeks of intragastric administration of normal saline (1.0 ml/kg/day), polyene phosphatidylcholine (PPC; 123.1 mg/kg/day) and TEL (8 mg/kg/day). The liver tissue was then assessed for the NAFLD activity score and fibrosis score (FS), and serum biochemistry and leptin levels were determined. Additionally, leptin protein expression levels were examined by western blotting and the expression of leptin mRNA was investigated by reverse transcription-polymerase chain reaction. TEL significantly improved FS in rats (P<0.01) and was more effective than PPC. TEL significantly reduced the expression of serum leptin, as well as the expression levels of leptin protein and its mRNA in liver tissue (P<0.01); however, the effects of PPC were not significant (P>0.05). TEL reduced serum leptin, leptin protein and its mRNA in the liver tissue of NAFLD rats, and improved the pathological indicators of liver fibrosis.

目的 研究替米沙坦对非酒精性脂肪肝大鼠炎症反应及肝纤维化的影响.方法 雄性SD大鼠以高脂饲料喂养12周造模,正常组(n=10)以普通饲料喂养12周.模型大鼠按照体重随机分为3组:模型组(n=15,1.0mL·kg-1 ·d-1生理盐水)、对照组(n=10,8.4 mg· kg-1·d-1多烯磷脂酰胆碱)和实验组(n=10,8 mg·kg-1 ·d-1替米沙坦),并继续给予高脂饲料喂养.16周后处死大鼠,用全自动生化分析仪检测血清谷丙转氨酶(ALT)、谷草转氨酶(AST)、三酰甘油(TG)、总胆固醇(TC)、白细胞介素-6(IL-6)、IL-8和肿瘤坏死因子-α(TNF-α)水平及大鼠肝组织性形态学变化.结果 给药16周大鼠体重,模型组为(582.63±33.59)g,正常组为(484.82±33.69)g,组间比较差异有统计学意义(P＜0.001).对照组及实验组大鼠体重分别为(538.54±39.46),(532.71±40.85)g,与模型组比较差异有统计学意义(P＜0.01).模型组大鼠肝指数为4.01 ±0.15,正常组为2.98±0.29,组间比较差异有统计学意义(P＜0.00).对照组的肝指数为3.54 ±0.12、实验组为3.65 ±0.13,与模型组比较差异有统计学意义(均P ＜0.001).与模型组小叶内炎症为2.80±0.42、NSA评分为7.70±0.48及纤维化11.25±2.12相比,对照组的小叶内炎症1.42 ±0.71、NSA评分5.71±0.50及纤维化9.11±2.03,组间比较差异有统计学意义(P ＜0.001,P＜0.001,P＜0.05).正常组血清ALT为(40.82±8.74)U·L-1、AST为(93.20±12.11)U·L-1、TG为(0.60±0.17) mmol·L-1、TC为(1.33±0.24) mmol·L-1,模型组分别为(112.12±23.40)U·L-1,(248.21±24.77)U·L-1,(0.78±0.21) mmol·L-1,(2.52±0.13)mmol·L-1,组间比较差异有统计学意义(P＜ 0.001,P＜0.001,P＜0.05,P＜0.001).实验组的ALT(87.11±12.05)U·L-1和AST(154.32±24.87)U·L-1,与模型组比较差异有统计学意义(P ＜0.01,P＜0.001).模型组血清IL-6为(151.38±30.67)pg·mL-1、IL-8为(1.26 ±0.27)ng·nL-1及TNF-α为(4.33±1.30)ng·mL-1,正常组分别为(66.83±15.08) pg·mL-1、(0.71±0.27)ng·mL-1、(1.46±0.45) ng·mL-1,组间比较差异有统计学意义(均P＜0.001).对照组IL-6为(110.17±23.60) pg·mL-1、IL-8为(0.89±0.24) ng·mL-1及TNF-α为(2.50±0.50) ng·mL-1,与模型组比较差异有统计学意义(均P ＜0.001);实验组IL-6为(100.42±15.10) pg·mL-1、IL-8为(0.90±0.16)ng·mL-1及TNF-α为(3.16 ±0.35)ng·mL-1,与模型组比较差异有统计学意义(P＜0.001,P＜0.001,P＜0.01).结论 替米沙坦可降低非酒精性脂肪肝大鼠肝症反应及肝纤维化进程.

OBJECTIVE To investigate the effects of telmisartan on expression of resistin in serum and liver under conditions of nonalcoholic steatohepatitis (NASH) and insulin resistance using a rat model system. METHODS Forty-five male Sprague-Dawley rats were randomly divided into a normal control group (NC, n=10), a model control group (MC, n=15), a polyene phosphatidylcholine prevention group (PP, n=10), and a telmisartan prevention group (TP, n=10). The NC group was given a standard diet and the other groups were given a high-fat diet for 16 weeks in order to induce NASH. At the end of week 12, 5 rats in the MC group were sacrificed for pathology confirmation of the NASH model. At the end of week 12, the TP group was given telmisartan (8.0 mg/kg/d) and the PP group was given polyene phosphatidylcholine (8.4 mg/kg/d) for an additional 4 weeks by intragastric administration. At the end of week 16, all rats were sacrificed and body weights recorded. Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol (TC), triglycerides (TG), resistin, insulin and fasting blood glucose were measured. The insulin resistance value, HOMA-IR, was assessed by homeostasis mode assessment. Liver expression of the resistin protein was detected by western blotting and of the resistin mRNA was detected by RT-PCR. The F test and LSD test were used for statistical analyses. RESULTS Compared to the NC group, the body weight and HOMA-IR of rats in the MC group were significantly increased (P<0.01). The levels of serum resistin, and of resistin protein and mRNA in liver, were significantly higher in the MC group than in the NC group of rats (all P less than 0.01). The body weight of rats in the TP group was significantly lower than those in the MC group (P<0.05). The levels of serrn resistin, resistin protein and mRNA in the liver, and insulin resistance were significantly lower in the TP group than in the MC group of rats (all P<0.01). The PP group did not show significant differences in any of these measures, except for loss of body weight (P<0.05). CONCLUSION Telmisartan elicits preventive and protective effects in a NASH rat model.Telmisartan may improve insulin resistance in NASH rats by decreasing the expression of serum resistin, and liver resistin protein and mRNA.

目的 探讨氯吡格雷及氯吡格雷联合阿司匹林对实验大鼠胃黏膜的影响及可能机制.方法 雄性SD大鼠随机分为4组,每组48只,分别予氯呲格雷、阿司匹林、氯吡格雷联合阿司匹林和生理盐水灌胃.给药前及给药后3、7、14、21和28 d处死大鼠,取胃观察.Guth法测定溃疡指数;免疫组织化学法测定胃黏膜TNF-α、VEGF表达.结果 氯吡格雷灌胃后大鼠胃黏膜损伤指数与对照组及用药前相比存在差异(P＜0 05).氯吡格雷联合阿司匹林灌胃后大鼠胃黏膜损伤指数与对照组及用药前相比,损伤存在差异(P＜0.01),与阿司匹林组及氯吡格雷组亦有差异(P＜0.01).TNF-α定量结果显示,各实验组用药后不同时间点与对照组或用药前比较,呈高水平表达,差异有统计学意义(P＜0.05).氯吡格雷组TNF-α表达与损伤指数呈正相关(P＜0.01).VEGF定量结果显示,各实验组用药后不同时间点与对照组或用药前比较,VEGF表达差异有统计学意义(P＜0.05).结论 常规剂量氯吡格雷可导致大鼠胃黏膜损害,胃黏膜VEGF表达减少,TNF-α表达增强.氯吡格雷联合阿司匹林对大鼠胃黏膜的损伤较单用氯吡格雷或阿司匹林明显加重.

Objective To investigate the effects of telmisartan on insulin resistance and oxidative stress in nonalco?holic steatohepatitis (NASH) rats. Methods Fifty male SD rats were randomly divided into five groups:control group, mod?el group, polyene phosphatidylcholine group, low-dose telmisartan group and high-dose telmisartan group by using random number table (n=10 in each group). Control group was given standard food,the other groups were given high fat diet for 12 weeks to establish NASH rat model. Then intervention groups were given either normal saline 1.0 mL/(kg·d) or polyene phos?phatidylcholine 8.4 mg/(kg·d), or telmisartan 4 mg/(kg·d) or telmisartan 8 mg/(kg·d) for 4 weeks by intragastric adminstra?tion. All rats were sacrificed at the end of the 16th week, the lever of plasma insulin resistance index (HOMA-IR), ALT, AST, TG, TC, MDA, SOD, T-AOC, CAT, GSH-PX and liver homogenate MDA, SOD, GSH-PX and liver NAS scores were tested. Results In polyene phosphatidylcholine treated group, the lever of plasma ALT, AST, HOMA-IR and liver NAS scores were degreased significantly compared with model group. The lever of plasma AST, SOD, T-AOC, CAT, GSH-PX and liver homogenate SOD, GSH-PX, liver NAS scores were improved in both low-dose and high-dose telmisartan groups com?pared with model group while plasma and liver homogenate MDA , HOMA-IR were reduced significantly in these two groups compared with model group. Besides, plasma ALT was significantly improved in high-dose telmisartan group compared with model group. Conclusion Telmisartan reduce plasma ALT, AST, oxidative stress, HOMA-IR and liver NAS scores in NASH rats. And high-does telmisartan is better than low-dose telmisartan and polyene phosphatidylcholine in treatment ef?fect.