Recently, many Chinese doctors have treated metabolic syndrome from pathogenic phlegm, dampness, stasis and heat, which not only meets the theory of TCM, but also has achieved good clinical effects, besides the method has been confirmed by animal experiments..

BACKGROUND:The establishment of a safe, reliable and easily repeatable mouse model of nonalcoholic fatty liver disease is the prerequisite for the study of the diagnosis and treatment of the disease.
OBJECTIVE:To establish a C57BL/6 mouse model of nonalcoholic fatty liver disease and observe changes of biochemical indicators, which can provide a theoretical basis for its pathogenesis and drug treatment.
METHODS:Sixty healthy male C57BL/6 mice were randomly divided into a control group of 30 cases (normal diet), and a model group of 30 cases (high fat diet). Models of nonalcoholic fatty liver were established. At 8 weeks, body mass, liver index, and homogenate superoxide dismutase activity in the liver were detected. Changes in serum alanine aminotransferase, aspartate aminotransferase, triglyceride glycerol, cholesterol, high-density lipoprotein cholesterol and low-density lipoprotein cholesterol were observed. Pathological examination was performed.
RESULTS AND CONCLUSION:(1) Pathological sections showed that large droplets and smal lipid droplets in the mouse liver and spread the whole liver. Swel ing of the liver cel s, visible cytoplasmic vacuoles and obviously inflammatory changes in liver cel s were observed in the model group. (2) Body weight and liver index were significantly higher in the model group than in the control group (P<0.05). Superoxide dismutase activity was significantly reduced in the liver (P<0.05). (3) Triglycerides, cholesterol, and low-density lipoprotein cholesterol levels were significantly higher, but high-density lipoprotein cholesterol levels were significantly lower in the model group than in the control group (P<0.05). (4) Nonalcoholic fatty liver mouse model is ideal for high-fat diet-induced animal model. The method is simple, repetitive, and can provide a stable animal model for the study on the mechanism of nonalcoholic fatty liver disease and drug treatment.

Objective To investigate the effects of Furong-Tongmai capsules on the expressions of interleukin-1 (IL-1) and tumor necrosis factor-α (TNF-α) in the sciatic nerve in diabetic rats.Methods A total of 50 rats were randomly divided into the normal control group,model group,and low-,medium-,and high-dose of Furong-Tongmai groups,10 rats in each group.Diabetes mellitus in rats were induced by intraperitoneal streptozotocin injection (60 mg/kg).The rats in the low-,medium-,and high-dose of Furong-Tongmai groups were intragastric administrated with Furong-Tongmai suspension 0.7,1.4 and 2.8 g/kg daily for 8 weeks,respectively.The rots in the normal control group and model group were intragastric administrated with equal-volume normal saline daily for 8 weeks.The expression levels of IL-1 and TNF-α in the sciatic nerve were detected with immunohistochemistry staining.Results The expression levels of IL-1 (1.43％ ± 0.17％ vs.0.21％ ± 0.09％;P＜0.05) and TNF-α (1.98％ ± 0.12％ vs.0.35％ ± 0.03％;P＜0.05) in the model group were significantly increased than those in the normal control group.The expression levels of IL-1 (0.54％ ± 0.14％,0.51％ ± 0.13％ vs.1.43％ ± 0.17％;all P＜0.05) and TNF-α (0.57％ ± 0.17％,0.49％ ± 0.15％ vs.1.98％ ± 0.12％;all P＜0.05) in the medium-,and high-dose of Furong-Tongmai groups were significantly decreased than those in the model group and low-dose of Furong-Tongmai group (1.08％ ± 0.18％ in IL-1,1.11％ ± 0.09％ in TNF-α;all P＜0.05).Conclusion Furong-Tongmai capsules can reduce the expressions of IL-1 and TNF-α in sciatic nerve in diabetic rats.

Objective To explore the the influence ofFurong-Tongmai capsules on myocardial expression of LN and CollagenⅢ in diabetes mellitus (DM) rats.Methods A total of 60 rats were randomly divided into the control group, the model group, the low-, middle- high-dosageFurong-Tongmai capsules group (n=10). The low-, middle-high-dosageFurong-Tongmai group was given 1.4, 0.7, 2.8 g/(kg body weight) Furong-Tongmai capsules. The other two groups were given the same dose of purified water. After 8 weeks treatment, the myocardial was taken to make pathology slice with SP immunohistochemistry staining. The expression of LN and CollagenⅢ were detected.Results Compared with model group, the expression of LN (0.67% ± 0.04%,0.65% ± 0.09%vs. 1.08% ± 0.13%) and CollagenⅢ (0.67% ± 0.15%, 0.69% ± 0.13%vs. 1.17% ± 0.12%) in the middle-high-dosageFurong-Tongmai groups significantly decreased (P<0.05). However, there were no statistical differences between the low-, middle- high-dosageFurong-Tongmai groups and the model group (P>0.05).Conclusions TheFurong-Tongmai capsules could inhibit the expression of LN and CollagenⅢ in DM rats.

Objective:To explore the material basis and potential mechanism of Sanhuang Yishen Capsules in the treatment of diabetes through network pharmacology, molecular docking and experimental verification.Methods:The active components and targets of Sanhuang Yishhen Capsules were screened using China Natural product chemical composition database and SymMap database, and the related targets of T2DM were screened by GeneCards database. The "Chinese materia medica-active component-target" network was constructed, and the intersection genes were enriched by GO and KEGG using R language. Key active components were selected for molecular docking verification with potential core targets. 60 rats were divided into normal group, model group, and Sanhuang Yishen Capsules group according to random number table method, with 15 rats in each group. In addition to the normal group, the diabetic rat model was prepared in the other groups, and the corresponding drugs were intragastric in each group for 8 weeks. The levels of fasting blood glucose (FBG), fasting insulin (FINS) and insulin resistance index (HOMA-IR) were measured by radioimmunoassay. Western blotting was used to detect protein expressions of epidermal growth factor receptor (EGFR), epidermal growth factor (EGF), Akt serine/threonine kinase 1 (AKT1), recombinant tumor protein p53 (TP53), and recombinant caspase 3 (CASP3).Results:A total of 160 active components and 298 targets of Sanhuang Yishen Capsules, 2194 targets related to T2DM, and 166 intersection targets were obtained. GO and KEGG analyzed a series of biological reaction processes mainly involved in signal transduction, oxidative stress, apoptosis, etc., and mainly involved in the regulation of P13K/Akt, P53, CASP3 and other targets. The results of molecular docking showed that the main active components obtained by screening had strong binding with the target. Compared with model group, FBG, FINS, HOMA-IR, TP53 and CASP3 in Sanhuang Yishen Capsules group decreased ( P<0.05), EGFR, EGF and Akt1 proteins increased ( P<0.05). Conclusion:The mechanism of Sanhuang Yishen Capsules for the treatment of may be related to the regulation of EGF/EGFR/P13K/Akt signaling pathway, TP53 signaling pathway, CASP3 signaling pathway, PPARG signaling pathway, ESR1 signaling pathway, PTGS2 signaling pathway, CAT signaling pathway and CTNNB1 signaling pathway.