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糖肝健治疗 2 型糖尿病非酒精性脂肪肝的作用机制。

Mechanism of TangGanJian on nonalcoholic fatty liver disease with type 2 diabetes mellitus.

机构信息

a Science and Education Department , Wuhan Hospital of Traditional Chinese Medicine , Wuhan , PR China.

b Post-Doctoral Research Center of Mayinglong Pharmaceutical Group Co., Ltd. , Wuhan , PR China.

出版信息

Pharm Biol. 2018 Dec;56(1):567-572. doi: 10.1080/13880209.2018.1504972.

Abstract

CONTEXT

TangGanJian (TGJ) has a curative effect in the clinical treatment of nonalcoholic fatty liver disease (NAFLD) with type 2 diabetes mellitus (T2DM), while the mechanism involved in the treatment process remains unclear.

OBJECTIVE

This study details the mechanism of TGJ on the treatment of NAFLD with T2DM.

MATERIALS AND METHODS

NAFLD was induced in T2DM rat model. Male Wistar rats were assigned into six groups: Group I (control), Group II (model), Group III (pioglitazone, 0.5 mg/kg), Group IV (high dose of TGJ, 24.8 g/kg), Group V (middle dose of TGJ, 12.4 g/kg) and Group VI (low dose of TGJ, 6.2 g/kg). All rats in each group were treated with the corresponding drugs by gavage for 8 weeks. Haematoxylin and eosin analysis was conducted. The indicators of inflammatory and oxidative stress were analysed utilizing one-way ANOVA.

RESULTS

The contents of TNF-α (15.794 ± 3.302 pg/mL), IL-6 (76.801 ± 8.491 pg/mL), IL-1β (100.101 ± 13.150 pg/mL), CRP (1.052 ± 0.079 pg/mL) and MDA (3.972 ± 0.159 pg/mL) were obviously elevated in NAFLD with T2DM rats compared to controls. Except for the IL-6, the levels of other markers declined in a dose-dependent manner after treatment with TGJ. The SOD (14.139 ± 1.479 U/mgprot) and GSH-PX (81.511 ± 5.276 U/mgprot) levels significantly decreased in NAFLD with T2DM rats, while the levels of these indicators increased after treatment with TGJ.

CONCLUSIONS

TGJ may be a therapy for the NAFLD with T2DM rats by modulating the inflammatory response and the oxidative stress capacity.

摘要

背景

糖肝健(TGJ)在治疗 2 型糖尿病合并非酒精性脂肪性肝病(NAFLD)方面具有疗效,但具体的治疗机制仍不清楚。

目的

本研究详细阐述了 TGJ 治疗 2 型糖尿病合并非酒精性脂肪性肝病的作用机制。

材料与方法

通过建立 2 型糖尿病大鼠模型诱导非酒精性脂肪性肝病,将雄性 Wistar 大鼠分为六组:I 组(对照组)、II 组(模型组)、III 组(吡格列酮,0.5mg/kg)、IV 组(TGJ 高剂量组,24.8g/kg)、V 组(TGJ 中剂量组,12.4g/kg)和 VI 组(TGJ 低剂量组,6.2g/kg)。每组大鼠均灌胃给予相应药物,连续治疗 8 周。采用苏木精-伊红染色进行病理学分析。采用单因素方差分析检测炎症和氧化应激相关指标。

结果

与对照组相比,2 型糖尿病合并非酒精性脂肪性肝病大鼠的 TNF-α(15.794±3.302pg/mL)、IL-6(76.801±8.491pg/mL)、IL-1β(100.101±13.150pg/mL)、CRP(1.052±0.079pg/mL)和 MDA(3.972±0.159pg/mL)含量明显升高。除 IL-6 外,TGJ 治疗后这些标志物的水平呈剂量依赖性下降。与对照组相比,2 型糖尿病合并非酒精性脂肪性肝病大鼠的 SOD(14.139±1.479U/mgprot)和 GSH-PX(81.511±5.276U/mgprot)水平显著降低,而 TGJ 治疗后这些指标水平升高。

结论

TGJ 可能通过调节炎症反应和氧化应激能力来治疗 2 型糖尿病合并非酒精性脂肪性肝病大鼠。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89fc/6249541/947caa7d1608/IPHB_A_1504972_F0001_C.jpg

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