ObjectiveTo investigate the therapeutic effects and mechanisms of Qinlian Hongqutang （QLHQT） on nonalcoholic steatohepatitis （NASH）. MethodsC57BL/6J mice were randomly divided into normal and modeling groups. The NASH model was established by feeding a high-fat diet for 12 weeks. After successful modeling， mice were randomly assigned to the model group， low-， medium-， and high-dose QLHQT groups （0.51， 1.02， and 2.04 g·kg^-1）， and a positive control metformin group， with six mice in each group. The mice were treated for 8 weeks. Body weight was recorded before and after treatment. Serum levels of total cholesterol （TC）， triglycerides （TG）， and low-density lipoprotein cholesterol （LDL-C）， as well as hepatic TC， TG， and LDL-C contents， were determined by biochemical assays. Hematoxylin-eosin （HE） staining and oil red O staining were used to evaluate liver histopathology and lipid deposition， respectively. Flow cytometry， enzyme-linked immunosorbent assay （ELISA）， and Real-time polymerase chain reaction （Real-time PCR） were used to assess hepatic macrophage expression and related markers. Western blot and immunofluorescence were used to investigate the potential mechanisms of QLHQT in regulating macrophage polarization. ResultsCompared with the normal group， body weight and serum and hepatic levels of TC， TG， and LDL-C were significantly increased in the model group （P<0.01）. Liver histopathology showed unevenly distributed round lipid droplets in the hepatocyte cytoplasm， accompanied by inflammatory cell aggregation. Flow cytometry showed that the proportion of CD86-positive cells was significantly increased， whereas the proportion of CD206-positive cells was markedly decreased （P<0.05）. Hepatic inducible nitric oxide synthase （iNOS） levels and tumor necrosis factor-α （TNF-α） mRNA expression were significantly increased， while hepatic IL-10 levels and IL-4 mRNA expression were significantly decreased （P<0.01）. The protein expression levels of Toll-like receptor 4 （TLR4）， tumor necrosis factor receptor-associated factor 6 （TRAF6）， and myeloid differentiation factor 88 （MyD88） in the liver were significantly increased （P<0.01）. Compared with the model group， body weight was reduced in the high-， medium-， and low-dose QLHQT groups and in the metformin group. Serum and hepatic TC， TG， and LDL-C levels were significantly decreased （P<0.01）. Liver histopathology showed alleviated hepatic lipid deposition， with markedly reduced lipid droplets and inflammation. Immunofluorescence and flow cytometry showed that the proportions of CD86-positive cells were significantly decreased， whereas the proportions of CD206-positive cells were significantly increased in the high-， medium-， and low-dose QLHQT groups （P<0.05）. Hepatic iNOS levels and TNF-α mRNA expression were significantly decreased （P<0.01）， whereas hepatic IL-10 levels and IL-4 mRNA expression were significantly increased （P<0.01）. The hepatic protein expression levels of TLR4， TRAF6， and MyD88 were significantly decreased， while signal transducer and activator of transcription 6 （STAT6） phosphorylation was significantly increased （P<0.05， P<0.01）. There was no statistically significant difference in total STAT6 protein expression. ConclusionQLHQT effectively ameliorates hepatic inflammation in NASH mice， and the mechanism may involve STAT6- and TLR4-mediated signaling pathways driving polarization of M1 macrophages toward the M2 phenotype.

ObjectiveTo investigate the therapeutic effects and mechanisms of Qinlian Hongqutang （QLHQT） on nonalcoholic steatohepatitis （NASH）. MethodsC57BL/6J mice were randomly divided into normal and modeling groups. The NASH model was established by feeding a high-fat diet for 12 weeks. After successful modeling， mice were randomly assigned to the model group， low-， medium-， and high-dose QLHQT groups （0.51， 1.02， and 2.04 g·kg^-1）， and a positive control metformin group， with six mice in each group. The mice were treated for 8 weeks. Body weight was recorded before and after treatment. Serum levels of total cholesterol （TC）， triglycerides （TG）， and low-density lipoprotein cholesterol （LDL-C）， as well as hepatic TC， TG， and LDL-C contents， were determined by biochemical assays. Hematoxylin-eosin （HE） staining and oil red O staining were used to evaluate liver histopathology and lipid deposition， respectively. Flow cytometry， enzyme-linked immunosorbent assay （ELISA）， and Real-time polymerase chain reaction （Real-time PCR） were used to assess hepatic macrophage expression and related markers. Western blot and immunofluorescence were used to investigate the potential mechanisms of QLHQT in regulating macrophage polarization. ResultsCompared with the normal group， body weight and serum and hepatic levels of TC， TG， and LDL-C were significantly increased in the model group （P<0.01）. Liver histopathology showed unevenly distributed round lipid droplets in the hepatocyte cytoplasm， accompanied by inflammatory cell aggregation. Flow cytometry showed that the proportion of CD86-positive cells was significantly increased， whereas the proportion of CD206-positive cells was markedly decreased （P<0.05）. Hepatic inducible nitric oxide synthase （iNOS） levels and tumor necrosis factor-α （TNF-α） mRNA expression were significantly increased， while hepatic IL-10 levels and IL-4 mRNA expression were significantly decreased （P<0.01）. The protein expression levels of Toll-like receptor 4 （TLR4）， tumor necrosis factor receptor-associated factor 6 （TRAF6）， and myeloid differentiation factor 88 （MyD88） in the liver were significantly increased （P<0.01）. Compared with the model group， body weight was reduced in the high-， medium-， and low-dose QLHQT groups and in the metformin group. Serum and hepatic TC， TG， and LDL-C levels were significantly decreased （P<0.01）. Liver histopathology showed alleviated hepatic lipid deposition， with markedly reduced lipid droplets and inflammation. Immunofluorescence and flow cytometry showed that the proportions of CD86-positive cells were significantly decreased， whereas the proportions of CD206-positive cells were significantly increased in the high-， medium-， and low-dose QLHQT groups （P<0.05）. Hepatic iNOS levels and TNF-α mRNA expression were significantly decreased （P<0.01）， whereas hepatic IL-10 levels and IL-4 mRNA expression were significantly increased （P<0.01）. The hepatic protein expression levels of TLR4， TRAF6， and MyD88 were significantly decreased， while signal transducer and activator of transcription 6 （STAT6） phosphorylation was significantly increased （P<0.05， P<0.01）. There was no statistically significant difference in total STAT6 protein expression. ConclusionQLHQT effectively ameliorates hepatic inflammation in NASH mice， and the mechanism may involve STAT6- and TLR4-mediated signaling pathways driving polarization of M1 macrophages toward the M2 phenotype.

This paper elaborated the research progress on transduction mechanisms of obese polycystic ovary syndrome (PCOS) and insulin resistance (IR). The action mechanisms of kidney-tonifying, spleen-invigorating and phlegm-resolving in the treatment of obese PCOS and IR were explored. It provided new ideas for the treatment of obese PCOS patients in the clinical practice of traditional Chinese medicine (TCM) gynecology. Literatures on TCM theories and modern signal pathways were used in the analysis of spleen-kidney deficiency and phlegm-dampness retention, which were the key pathogenesis of obese PCOS and IR. The scientific nature of treating obese PCOS and IR from the method of kidney-tonifying, spleen-invigorating and phlegm-resolving was demonstrated. The results showed that the scientific nature of treating obese PCOS and IR from the method of kidney-tonifying, spleen-invigorating and phlegm-resolving was initially demonstrated by the organic combination of TCM and modern medicine theories. It innovatively proposed that the treatment study strategy of transduction molecular mechanism took the interactive dialogue between PI-3K/Akt signal pathway and TNF-α signal pathway as its target. The regulatory role and action mechanism of this method in the treatment of obese PCOS and IR were discussed.

This study was aimed to establish and evaluate obese polycystic ovary syndrome (PCOS) rat model. Rats were randomly divided into the blank control group, high-fat model group, insulin (INS) combined human chorionic gonadotropin (HCG) model group, and INS combined HCG plus high fat emulsion model group. The obese PCOS rat model was induced by subcutaneous injection of INS and HCG on the nape, respectively. The intragastric administration of high fat emulsion was also used in the PCOS rat model establishment. The estrous cycle of rat was monitored. The detection was also made the weight increasing rate of rats, luteinizing hormone (LH), follicle-stimulating hormone (FSH), estradiol (E2), testosterone (T), high-density lipoprotein (HDL), low density lipoprotein (LDL), triglyceride (TG), cholesterol (TC), fasting plasma glucose (FPG), fasting insulin (FINS), 2 h blood glucose and 2 h INS. Calculation was made on the HOMA index, related viscera index and bilateral ovaries HE staining. The results showed that when INS combined HCG improved method (INS combined HCG plus high fat emulsion model group) rats were sacrificed, the body weight, weight increasing rate, ovary viscera index, T, LH, and HOMA index were significantly higher than that of the blank control group, high-fat model group and INS combined HCG model group (P < 0.05,P < 0.01); HDL was significantly decreased (P < 0.05,P < 0.01). FPG, FINS, and 2 h INS of the INS combined HCG improved method group were significantly higher than that of the high-fat model group (P <0.01). It was concluded that INS combined HCG improved method was one of the ideal animal model establishment methods in the pathogenesis study of PCOS.

ObjectiveTo investigate the control rate and influence factors of glycolated hemoglobin A1C(HbA1c) of type 2 diabetes in Baoding city community.MethodsA cluster-randomized study was conducted and three communities were selected randomly.The study involved all of people aged 45 years old and above in the three communities.The type 2 diabetic patients diagnosed before,were recorded through the cross section study.Then the questionnaire was finished.All diabetic plasma HbA1c was determined by HPLC method.ResultsEighty-seven patients with HbA1c≤7％ were only 18.6％ in all diabetic patients.As the plasma level of HbA1c increased,occurrences of macroangiopathy and microangiopathy were both increased,by the trend test.Logistic regression analysis showed that therapeutic measures and knowledge about diabetes were main influence factors of achieving the hemoglobin Alc target of ＜7％ in type 2 diabetes.ConclusionThere were low HbA1c control in diabetic patients of Baoding community,and knowing diabetes well and receiving insulin treatment might decrease HbA1c level apparently.

OBJECTIVE: A gargle was designed and prepared for treating immune inpairment and anaerobic infection of oral cavity .The method of its quantitative analysis was established and put into clinical use. METHODS: HPLC was used as the quantitative analysis method .The effect on oral lichen planus was clinically observed. RESULTS: The taste of the gargle was well acceptable, and its quality was well controlled.The cure rate for oral lichen planus was 96%. No adverse reactions were found. CONCLUSION: The taste and method of quantitative analysis are well acceptable. The clinical effect is satisfactory.