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Hyperglycemia is a typical pathogenic factor in a series of complications among patients with type II diabetes. Epigallocatechin-3-gallate (EGCG) is the major polyphenol extracted from green tea and is reported to be an antioxidant. The aim of the present study was to examine the effect of EGCG on insulin resistance in human HepG2 cells pretreated with high concentrations of glucose. The protein kinase B (AKT)/glycogen synthase kinase (GSK) pathways were analyzed using western blot analysis in HepG2 cells and primary mouse hepatocytes treated with high glucose and/or EGCG. Cellular glycogen content was determined using a glycogen assay kit. Reactive oxygen species (ROS) production was determined using dihydroethidium staining and flow cytometry. c‑JUN N‑terminal kinase (JNK)/insulin receptor substrate 1 (IRS1)/AKT/GSK signaling was explored using western blot analysis in HepG2 cells treated with high glucose and/or EGCG or N-acetyl-cysteine. High glucose significantly decreased the levels of phosphorylated AKT and GSK in HepG2 cells and mouse primary hepatocytes. Pretreatment with EGCG significantly restored the activation of AKT and GSK in HepG2 cells and primary hepatocytes exposed to high glucose. In HepG2 cells and primary hepatocytes, glycogen synthesis was improved by EGCG treatment in a dose‑dependent manner. High glucose significantly stimulated the production of ROS while EGCG protected high glucose‑induced ROS production. ROS is known to serve a major role in high glucose induced‑insulin resistance by increasing JNK and IRS1 serine phosphorylation. In the present study, EGCG was observed to enhance the insulin‑signaling pathway. EGCG ameliorated high glucose‑induced insulin resistance in the hepatocytes by potentially decreasing ROS‑induced JNK/IRS1/AKT/GSK signaling.

Essential hypertension (EH) was a complex disease resulted from the interaction of cumulative effect of multiple genetic and environment factors. The relationship between the genetic polymorphisms in the transforming growth factor-beta1 (TGF-beta1), the blood levels and EH have been investigated, but the conclusions were different. Therefore, we investigate the relationship between the tagging single nucleotide polymorphisms (tSNPs) (rs1800469, rs2241716, rs11466345, rs2241715, rs4803455) in TGF-beta1 gene, blood levels and EH in the Han nationality population in Xinjiang, to clarity the pattern of linkage disequilibrium (LD) and the feature of the structure of haplotype.Based on the case-control study,we selected 732 (365 EH patients,367 controls) Han Chinese population from the Boertonggu countryside of Shawan region in the Xinjiang Uygur Autonomous Region of China by random cluster sampling. After questionnaire and physical examination, we collected blood samples, and the blood levels of TGF-beta1 were quantified using sandwich ELISA. The polymorphisms of TGF-beta1 gene in the study groups were detected with SNaPshot system. The case-control study in a large group was carried out separately for each of the tSNP and followed up by haplotypes analyses to determine the relation between tSNPs of TGF-beta1 gene and EH in the Han population.(1) The frequencies of alleles A, G of rs11466345 of TGF-beta1 gene in EH group and control group were as follows: 69.7%, 30.3%, 74.4%, 25.6%, respectively. It was demonstrated that the G allele of the rs11466345 polymorphism occurred at a significantly higher frequency in EH patients than in healthy controls (30.3% vs. 25.6%, P0.05). The rs11466345G-allele carriers had a significantly increased risk of EH compared to rs11466345A-allele carrier (OR = 1.261; P0.05). The frequencies of genotypes and alleles of the other tSNPs of TGF-beta1 gene had no difference between EH patients and controls (P0.05). (2)Except the site of rs11466345, the other tSNPs were in strong LD, and no statistical differences were observed in haplotypes distribution in the followup study between case-control groups (P0.05). (3) There were no difference of TGF-beta1 levels between the different genotypes and alleles in tSNPs of TGF-beta1 gene (P0.05).(1) These results suggested that TGF-beta1 gene rs11466345 G allele was likely to be a genetic susceptibility factor for EH in the Xinjiang Han population, the other tSNPs perhaps had no association with EH of in the study groups. (2) Except rs11466345, the other tSNPs were in strong LD, and the haplotypes reconstructed by tSNPs might not be associated with EH in the Han nationality populations. (3) There was no association between the tSNP of TGF-beta1 gene and TGF-beta1 blood levels in the Xinjiang Han nationality population.

To investigate the association of the transforming growth factor- beta 1 (TGF- beta 1) gene polymorphisms and blood TGF- beta 1 level with essential hypertension (EH) in Kazakh Chinese.The polymorphisms of TGF- beta 1 gene in 354 Kazakh EH patients and 435 healthy controls were detected with polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and DNA sequencing. The blood level of TGF- beta 1 was quantified using specific sandwich ELISA.The frequencies of genotypes GG, GC and alleles G and C of +915G/C in Xinjiang Kazakh were 97.9%, 2.1% and 98.77%, 1.23%, respectively. No significantly difference was found between EH patients and controls (P0.05). The frequencies of genotypes TT, TC, CC and alleles T and C of +869T/C in controls was 25.97%, 46.67%, 27.36%, 49.3% and 50.7%, respectively, the CC genotype or C allele in EH patients had significantly higher frequencies than controls [41.60% vs. 27.36%, and 62.2% vs. 50.7%, respectively (P0.05)]. It was also shown that TGF- beta 1 +869 C allele carriers had significantly increased risk of EH compared with T allele carriers (OR=1.60, P=0.00). There was linkage disequilibrium (LD) between the two polymorphisms. The frequency of haplotype C-G in the EH group was significantly higher than that in controls (61.6% vs. 49.8%, P0.05). There were no differences in TGF- beta 1 level among different genotypes or alleles in both +869T/C and +915G/C loci (P0.05).The frequency of +915G/C variation of the TGF- beta 1 gene was very low in Kazakh and there was no homozygous variation. The +869 C allele was likely the genetic susceptibility factor for EH in the population. There was linkage disequilibrium in the polymorphisms of +869T/C and +915G/C. Haplotype C-G was the risk factor of EH.

Based on a case-control study, we investigated the relationship between +869T/C and +915G/C gene polymorphisms in transforming growth factor-beta1 (TGF-beta1), protein levels and essential hypertension (EH) in the Kazakh and Han Chinese populations selected from the Boertonggu countryside of Shawan region in the Xinjiang Uygur Autonomous Region of China (n=1600). The polymorphisms of TGF-beta1 and the blood levels were detected using polymerase chain reaction-restriction fragment length polymorphism assays and sandwich ELISA, respectively.An association was found between +869C-allele with higher risk of EH in these two populations. We also found that the CG haplotype of the two polymorphisms was associated with EH in the Kazakh EH patients. The levels of TGF-beta(1) in the blood were positively correlated with diastolic blood pressure both in the Kazakh and Han EH patients. Levels of the TGF-beta1 protein in the Kazakh EH patients were significantly higher than those in the Han EH patients.These results suggest that the TGF-beta1 +869 C allele is potentially a genetic factor of EH in these two ethnicities, the CG haplotype can be a genetic marker of EH in the Kazakh Chinese and the high concentration of TGF-beta1 is possibly associated with EH, especially in the Kazakh population.