Di'ao Xinxuekang alleviates non-alcoholic steatohepatitis in mice by up-regulating Nrf2/HO-1 signaling pathway / 中国中药杂志

The present study investigated the therapeutic effect and mechanism of Di'ao Xinxuekang(DXXK) on non-alcoholic steatohepatitis(NASH) in mice. Sixty-five C57 BL/6 J mice were randomly divided into a normal group and an experimental group for model induction with the high-fat diet for 16 weeks. Then the mice in the experimental group were randomly divided into a model group, an atorvastatin group(4 mg·kg~(-1)·d~(-1)), and high-(200 mg·kg~(-1)·d~(-1)), medium-(60 mg·kg~(-1)·d~(-1)), and low-dose(20 mg·kg~(-1)·d~(-1)) DXXK groups, with 10 mice in each group. Drugs were administered by gavage for eight weeks. Serum lipid, liver lipid, serum alanine aminotransferase(ALT), aspartate aminotransferase(AST), malondialdehyde(MDA), superoxide dismutase(SOD), and glutathione reductase(GSH-Px) were determined. Interleukin-1β(IL-1β) and tumor necrosis factor-α(TNF-α) were measured by enzyme-linked immunosorbent assay(ELISA). The liver index was calculated. The liver pathological change and lipid accumulation were observed by HE and oil red O staining. The liver ultrastructure was observed by the transmission electron microscope. The mRNA and protein expression of nuclear factor-erythroid 2 related factor 2(Nrf2) and heme oxygenase-1(HO-1) was detected by real-time fluorescence-based quantitative PCR and Western blot, respectively. The results showed that compared with the normal group, the model group displayed serum lipid and liver lipid metabolism disorders, elevated transaminase, lipid deposition, steatosis, and inflammation, suggesting that the NASH model in mice was properly induced. Compared with the model group, the DXXK groups showed decreased serum lipid, liver lipid, ALT, AST, MDA, IL-1β, and TNF-α, increased SOD and GSH-Px, alleviated hepatic steatosis, ballooning, and inflammation, and up-regulated Nrf2 and HO-1 gene and protein expression. In conclusion, DXXK can significantly alleviate NASH in mice, which is related to the inhibition of oxidative stress and inflammatory damage by up-regulating the Nrf2/HO-1 signaling pathway.

Animal Models of Nonalcoholic Fatty Liver Disease：A Review / 中国实验方剂学杂志

Nonalcoholic fatty liver disease （NAFLD） is a metabolic stress-induced liver injury characterized by excessive lipid accumulation in hepatocytes， which is closely related to insulin resistance and genetic susceptibility. It falls into the category of "liver lump" in traditional Chinese medicine （TCM）. NAFLD affects about 25% of the population worldwide and has become a major burden of the world health care system. However， its exact pathogenesis remains unclear. Conducting the basic research on NAFLD is of great clinical significance and social value. As an important tool for NAFLD research， animal model plays a particularly important role in clarifying the pathophysiological mechanism of NAFLD. In recent years， the modeling methods for NAFLD in China and abroad have been constantly updated， and in particular， certain progress has been made in the duplication of TCM syndrome models. By consulting and sorting out the relevant literature published in recent years in China and abroad， the author summarized the replication methods of NAFLD animal models. This paper reviewed the advantages and disadvantages of models established via dietary induction （high-fat feed， high-fat and high-fructose feed， high-fat and high-cholesterol feed， and methionine choline-deficient feed）， models with genetic defects ［leptin-deficiency （Lepob/Lepob）， autosomal recessive diabetes gene homozygous deficiency （ob/ob）， Alms1 gene （foz/foz） mutation， and FATZO mice］ and exposure to special diets， and models for TCM syndromes （liver depression and spleen deficiency syndrome， phlegm-dampness syndrome， blood stasis syndrome， combined phlegm and stasis syndrome， and qi stagnation and blood stasis syndrome）， in order to provide reference for the preparation of more scientific， reasonable， economical， and convenient animal models of NAFLD， thus laying a foundation for in-depth study of the pathogenesis， prevention， and treatment of NAFLD.

Studies on antidiabetic effects of cortex Moutan polysaccharide-2b in type 2 diabetes mellitus rats / 药学学报

<p><b>AIM</b>To study the antidiabetic effects of cortex Moutan polysaccharide-2b (CMP-2b) in type 2 diabetes mellitus (T2DM) rats.</p><p><b>METHODS</b>The T2DM model rats were induced by a single intravenous injection of low dose streptozotocin (STZ) and intake of high sucrose-fat diet. CMP-2b was given to T2DM rats daily through gavage for 4-5 weeks. The body weight, water and food intake, fasting blood glucose (FBG), glucose tolerance, plasma lipids, serum insulin, and insulin receptor (Ins R) were determined.</p><p><b>RESULTS</b>Oral administration of CMP-2b significantly decreased water and food intake, FBG, total cholesterol (Tch), and triglyceride (TG), improved the impaired glucose tolerance (IGT), and remarkably raised the number of low affinity InsR and insulin sensitivity index (ISI) in T2DM rats.</p><p><b>CONCLUSION</b>CMP-2b may be useful for treating T2DM and its complications.</p>

Therapeutic effect of xinfeng capsule in treating adjuvant arthritis in rats and its effect on fas, fasL and bcl-2 expression in synovial membrane / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To observe the therapeutic effect of Xinfeng Capsule (XFC) in treating adjuvant arthritis of rats and its effect on fas, fasL and bcl-2 expression in synovial membrane.</p><p><b>METHODS</b>Rats were randomly divided into the normal group, the model group, the model group, the methotrexate (MTX) group, the TPT group and the XFC group. Except for the rats in the normal group, animals were modelled to adjuvant arthritis with Freund's complete adjuvant, and the latter three groups were treated with MTX, Tripterygium wilfordii polysaccharide (TPT) and XFC respectively. The arthritis index (AI), change of body weight (BW) of rats were recorded, and the expressions of fas, fasL and bcl-2 in rats' synovial membrane were determined.</p><p><b>RESULTS</b>Compared with before treatment, the AI in the three treated groups was lowered significantly (P < 0.01, P < 0.05). The BW increment in the XFC group after treatment was insignificantly different to that in the normal group (P > 0.05), while it was significantly lower in the other two treated groups than that in the normal group and the XFC group (P < 0.01). Compared with the model group, fasL expression was increased in the XFC group significantly (P < 0.05), but bcl-2 expression decreased, fas expression showed insignificant difference (P > 0.05). Comparison of the three gene expressions between the three treated groups showed no significant difference (P > 0.05).</p><p><b>CONCLUSION</b>XFC could decrease AI in rats with adjuvant arthritis in the same way as MTX and TPT, it effected better in increasing BW than the latter two. The effect of XFC might be performed by its action in enhancing fasL expression, inhibiting bcl-2 expression and promoting apoptosis of proliferated synovial membranous cell so as to restrain hyperplasia of synovial membrane.</p>