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Panax notoginseng saponins (PNS) are a commonly used traditional medicine to treat diabetes in China. Recent studies have confirmed their anti‐diabetic effects, but the underlying mechanisms have remained unclear. The present study was designed to explore whether PNS decrease hyperglycemia by improving insulin sensitivity in skeletal muscle and to elucidate the molecular mechanisms. The anti‐diabetic effects of PNS were analyzed in a skeletal myoblast cell line, C2C12, and in high fat diet‐induced diabetic KKAy mice. C2C12 cells were treated with PNS (50, 100, and 200 μg·L−1) and examined for glucose uptake, cell viability and expression of components of the phosphoinositide 3‐kinase (PI3K)–protein kinase B (AKT) signaling pathway. KKAy mice were intraperitoneally injected with PNS (200 mg·kg−1) for 6 weeks. Body weight, blood glucose, serum insulin, serum lipid, glucose and insulin tolerance were measured to evaluate the anti‐diabetic effects of PNS. Pathological changes, apoptosis and the PI3K–AKT signaling pathway were analyzed in KKAy skeletal muscle. PNS significantly increased insulin‐induced glucose uptake, but did not affect the cell viability of C2C12 cells. In addition, PNS reduced blood glucose and serum insulin levels and improved glucose tolerance and insulin tolerance of KKAy mice. Pathological changes and apoptosis of skeletal muscle were relieved by PNS treatment. Moreover, PNS treatment enhanced expression of mRNA encoding IRS1 and GLUT4, as well as the protein expression of phosphorylated (p) ‐insulin receptor substrate 1 (IRS1), p‐PI3K, p‐AKT and glucose transporter type 4 (GLUT4) in C2C12 and KKAy mouse muscle. Collectively, these data indicate that PNS reduces hyperglycemia and insulin resistance through up‐regulating GLUT4 expression and the IRS1–PI3K–AKT signaling pathway. Furthermore, PNS alleviated diabetes skeletal muscle pathological damage. Thus, our data suggest that PNS may be promising anti‐diabetic compounds.

OBJECTIVE To investigate the protective effects of Jiayan Kangtai (JYKT) granules, consisting of 9 Chinese herbs, in a rat model of autoimmune thyroiditis (AIT), and the possible underlying mechanism. METHODS Female Lewis rats (6–8 weeks) were randomly apportioned to 5 groups of 10, including a normal control. AIT was induced in the untreated AIT-model group, and rats treated subsequently with daily low, medium, or high dose JYKT granules. After 12 weeks, plasma levels of thyroid autoantibodies and morphological changes in the thyroid were detected by enzyme-linked immunosorbent assay and histological examination, respectively. The presence of interleukin (IL)-6, IL23p19, and IL-2 in thyroid tissue was assessed by immunohistochemical staining. The percentages of T helper (Th)17 cells and regulatory T cells (Tregs) in the peripheral blood were analyzed by flow cytometry. Relevant levels of cytokines and proteins were examined via bead-based multiplex flow cytometry and ELISA, respectively. Expressions of genes and proteins regulated by Th17 cells and Tregs were shown by real-time PCR and Western blot. RESULTS Compared to the control, AIT-model rats had higher plasma concentrations of thyroid autoantibodies. The high-dose JYKT rats showed significantly lower levels of thyroid autoantibodies compared with the AIT model group. Rats in the AIT-JYKT groups also had fewer thyroid lesions and less lymphocytic infiltration, a lower percentage of Th17 cells, and a higher percentage of Tregs, compared with the AIT-model. Rats given high-dose JYKT had a significantly lower Th17/Treg ratio compared with the AIT model. Differences in plasma cytokine concentrations and relevant gene and protein expressions in the spleens of JYKT-treated rats and the AIT group suggested an association between JYKT treatment and lower Th17 cell percentage and higher Treg activity. CONCLUSION JYKT treatment appeared to be protective against AIT in rats, possibly via the regulation of the Th17 cell/Treg imbalance in AIT.

OBJECTIVE To evaluate whether endothelial dysfunction and hypertension are prevented by trans-cinnamaldehyde (tCA) through the activation of endothelial nitric oxide synthase (eNOS). METHODS Human umbilical vein endothelial cells (HUVECs) were cultured in vitro and stimulated with tCA to determine cell viability using the methyl thiazolyl tetrazolium assay. The effect of tCA on nitric oxide (NO) production was determined by diaminofluorescein-dyes in the absence or presence of inhibitors of eNOS, AMPK, PKA, and AKT. The effect of tCA on blood pressure was determined by the tail-cuff method in obesity spontaneous hypertension (SHR. Cg-Leprcp/NDmcr) rats. The phosphorylation of eNOS and protein expression of the insulin-signaling pathway (InsR-IRS1-PI3K-AKT) were measured by western blot. RESULTS tCA at concentrations less than 100 did not affect cell viability in cultured HUVECs. Stimulation with tCA promoted NO release in a time-dependent manner compared with the control group. tCA-treated HUVECs also significantly increased AKT-Ser473 and eNOS- Ser1177 phosphorylation. In SHR-CP rats, treatment with tCA at a dose of 40 mg/kg/day for 6 weeks markedly reduced the systolic blood pressure and diastolic blood pressure, increased the phosphorylation of AKT and eNOS, and increased urinary nitric oxidation. CONCLUSION tCA attenuated endothelial dysfunction and reduced blood pressure in SHR-CP rats. The underlying mechanisms may involve the increase in AKT and eNOS phosphorylation and the release of eNOS-derived NO.

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-5's mechanism might be associated with its ability to activate the AdipoR2/AMPK pathway.

Objective To investigate the effects of Tangnaikang (TNK), a mixture of five herbal plant extracts, on inflammation-mediated insulin resistance and β-cell apoptosis in SHR.Cg-Lepr cp /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-Δ (TNF-Δ), 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 β-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 β-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-Δ, 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 β-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 β-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.

In large antenna arrays, the failure of some radiation elements is inevitable. In this case, the pattern is usually destroyed and the performance of array is mostly decreasing. In this paper, genetic algorithm is used to improve the similarity of the antenna pattern by optimizing the weight of the working array elements. When there are some interference signals, it can better recover the null. At the same time, the correlation coefficient can represent the similarity of two arrays. The mean of error can explain the error of the two array patterns, so the two numerical results can be used to evaluate the effect of optimization, and to illustrate the effectiveness of this method.