Liu Tonghua

Effect of lit-moxa stimulation of Guanyuan（CV 4） acupoint on levels of lactic acid and super-oxide dismutase in skeletal muscle of rats

OBJECTIVE To observe the effect of lit-moxa stimu- lating acupoint Guanyuan (CV 4) on lactic acid and super-oxide dismutase (SOD) in skeletal muscle after exercise exhaustion. METHODS Twenty-eight adult male Sprague-Dawley rats were randomly divided into normal control group, exhausted control group, exercise group and moxibustion group using exercise training and mild heating with lit-moxa stick as treatment methods. The exhausted control group, moxibustion group and exercise group received an exhaustive swimming after 20 days of intervention. Swimming exhausted times were recorded. Lactic acid and SOD concentration in soleus muscle were detected and compared between every two groups. RESULTS The swimming exhausted times of the moxibustion group and the exercise group were significantly increased compare to the exhausted control group (P < 0.05). The lactic acid of the exhausted control group was significantly increased comparing with the normal control group (P < 0.05), and the lactic acid of the moxibustion group and the exercise group were significantly lower than that of the exhausted control group (P < 0.05). The SOD level of the exhausted control group was significantly decreased comparing with the normal control group (P < 0.05), and the SOD level of the moxibustion group and the exercise group were significantly higher than that of the exhausted control group (both, P < 0.05). There was no statistical difference between the moxibustion group and the exercise group. CONCLUSION With lit moxa stick, heat stimulating acupoint of Guanyuan (CV 4) decreased the levels of lactic acid and SOD in rats skeletal muscle.

Tangnaikang improves insulin resistance and β-cell apoptosis by ameliorating metabolic inflammation in SHR.Cg-Lepr cp /NDmcr rats

OBJECTIVE To investigate the effects of Tangnaikang (TNK), a mixture of five herbal plant extracts, on inflammation-mediated insulin resistance and B-cell apoptosis in SHR.Cg-Leprcp/NDmcr (SHR-cp) rats. METHODS Seven-week-old SHR-cp rats were randomly divided into a control (CON) group and a TNK (3.24 g/kg) group. Wistar-Kyoto rats at the same age were used as the normal control group. After 7 weeks of continuous intragastric administration of TNK, the glucose metabolic status and insulin sensitivity of the rats were evaluated by assessing fasting serum glucose (FBG), the oral glucose tolerance test (OGTT), fasting serum insulin (FINS), and the insulin sensitivity index (ISI). Serum tumor necrosis factor-a (TNF-a), interleukin-6 (IL-6), C-reactive protein (CRP) and adiponectin were measured via enzyme-linked immunosorbent assays. Macrophage infiltration and apoptosis in adipose tissues were detected through F4/80 immunohistochemistry and the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Islet morphology and B-cell apoptosis were investigated using double immunofluorescence staining and the TUNEL assay. The expression of cytokine genes in adipose tissue, the liver, and the pancreas was detected in real-time polymerase chain reaction assays. The expression and phosphorylation levels of insulin signaling-, inflammation-, and B-cell survival-related proteins in the liver and pancreas of SHR-cp rats were detected by western blotting. RESULTS TNK (3.24 g/kg) treatment significantly decreased body weight, FBG and FINS; improved impaired glucose tolerance; increased the ISI; reduced serum levels of TNF-a, CRP and IL-6; and increased serum adiponectin. The mRNA expression of inflammatory markers was markedly reduced in the liver, pancreas, and adipose tissue. F4/80- and TUNEL-positive cells in adipose tissues were decreased, as was the number of TUNEL-positive B-cells. The phosphorylation of c-Jun N-terminal kinase and that of insulin receptor substrate-1 at serines 307 and 1101 was significantly decreased. In the pancreas, the expression of nuclear factor kappa-light chain-enhancer of activated B cells-p65 was significantly decreased, and phosphoinositide 3-kinase and IRS-2 were significantly increased. CONCLUSION TNK was able to improve insulin resistance and B-cell apoptosis in SHR-cp rats, which might be associated with its ability to relieve the overall and local metabolic inflammatory responses observed in SHR-cp rats.

Mixture of five herbal extracts ameliorates pioglitazone-induced aggravation of hepatic steatosis via activating the adiponectin receptor 2/AMP-activated protein kinase signal pathway in diabetic KKAy mice

Abstract Objective To assess the effect of a mixture of five herbal extracts (FT-5) on insulin resistance, glucose/lipid metabolism, hepatic steatosis, and to investigate whether the combination of FT-5 and pioglitazone would provide a robust effect on diabetes treatment, while may minimize undesirable side-effects of pioglitazone in diabetic Ay gene (KKAy) mice. Methods Seven-week-old KKAy mice were randomly divided into five groups: control (CON) group, FT-5 (2.0 g/kg) group, pioglitazone (20 mg/kg) (PIO) group, pioglitazone (20 mg/kg)+FT-5 (2.0 g/kg) (P+F) group. Age-matched C57BL/6J mice were used as the control group. After seven weeks of continuous intragastric administration of medication, the glucose metabolism, insulin sensitivity and lipid metabolism of KKAy mice were evaluated by assessing the fasting blood glucose (FBG), oral glucose tolerance test (OGTT), fasting serum insulin (FINS), insulin tolerance test (ITT), homeostasis model of assessment-insulin resistance index (HOMA-IR), total cholesterol (TC), total triglycerides (TG), and free fatty acids (FFA) in plasma and liver. Plasma and hepatic adiponectin were measured via enzyme-linked immunosorbent assays. Genes related to adipogenesis and lipolysis in white adipose tissues (WAT) and liver were examined by real-time polymerase chain reaction. Lipid metabolism-related protein expression in the liver of KKAy mice were detected by western blotting. Results PIO treatment remarkably improved insulin resistance. However, it also showed substantial side effects. FT-5 group exhibited no significant decrease in serum glucose. However, it reduced fasting plasma TG levels and improved hepatic steatosis of KKAy mice. P + F group showed improved insulin resistance and similar body weight gain, as compared with control group. The mRNA expression of genes related to fatty acid oxidation was markedly up-regulated in the liver of P + F group. Pioglitazone administration markedly decreased the phosphorylation levels of AMPK, as compared with all other groups. Besides, even though plasma adiponectin increased in PIO, FT-5, P + F group, adipoR2 gene expression significantly decreased in the liver of PIO group. Conclusion FT-5 decreased plasma TG and alleviated aggravating hepatic steatosis induced by pioglitazone in KKAy mice. FT-5s mechanism might be associated with its ability to activate the AdipoR2/AMPK pathway.