Ameliorative Effect ofGuava Leaf Total Flavonoids Reversing Insulin Resistance in Pancreaticβ Cells / 世界科学技术-中医药现代化

This study was aimed to observe the effect ofGuava leaf total flavonoids on HIT-T15 pancreaticβcell insulin resistance. Effective part of FSL was prepared. The dosing time, concentration and high glucose concentration of FSL were confirmed by observing HIT-T15 pancreaticβ cell growth curve and the influences of HIT-T15 pancreaticβ cell proliferation by different concentrations of glucose and FSL. Afterwards, the influence of FSL on HIT-T15 pancreaticβ cell insulin secretion, the expression of insulin receptor mRNA and insulin receptor substrate (IRS) 1 protein were measured under the environment of high glucose. The results showed that 50 mmol·L-1 glucose can significantly inhibit the proliferation of HIT-T15 pancreaticβ cell (P < 0.01). The 50μg·mL-1 FSL can significantly promote the proliferation of HIT-T15 pancreaticβ cells (P < 0.01), the insulin secretion (P < 0.05), the expression of insulin receptor mRNA (P < 0.05), and the protein expression of IRS 1 (P <0.01). It was concluded thatGuava leaf total flavonoids can promote the insulin secretion of HIT-T15 pancreaticβ cells under the circumstance of high concentration of glucose which may be related to its effect of increasing expression of insulin receptor mRNA and IRS-1 protein.

The Short Term Effect of Insulin on Proinsulin Gene Expression of HIT-T15 Insulinnoma Cells / 天津医药

Objective To investigate the short term effect of insulin on proinsulin gene expression of HIT-T15 insu-linnoma cells(pancreatic isletβ-cell). Methods The HIT-T15 cells were randomly divided into four groups.Blank Con-trol Group (LG):complete medium contain 1.4 mmol/L glucose. Control group (LGC):co-cultured nifedipine with medium in order to restain endogenous insulin release. Experimental group (LINS or HINS) add 0.5 U/L insulin or 5 U/L insulin on top of LGC. After being stimulated for 0, 30, 60, 90, 120 mins, proinsulin (PI) mRNA level were assessed by semi-quantitative RT-PCR. Insulin receptor substrate1 (IRS1) tyrosine phosphorylation was detected by immunocytochemistry. Results (1) Expression of PI was up regulated by both LINS and HINS, and peak at 60 mins. (2) After stimulation for 30 mins, the level of IRS1 tyrosine phosphorylation in the experimental group was significantly higher than control group, and the peak time be-tween LINS and HINS was different. (3) Between group of LG and LGC, the expression of PI mRNA and IRS1 tyrosine phos-phorylation show no difference. Conclusion Short term exogenous insulin stimulation can promote expression of proinsulin genes,which is concentration dependent. The expression and regulation of PI were related with IRS1 signal transduction.

Effect of ISL1 over-expression on proliferation of HIT-T15 cells / 中华内分泌代谢杂志

The effect of insulin gene enhancer binding protein (ISL1) on proliferation of HIT-T15 cells was investigated.ISL1 significantly promoted cell proliferation.ISL1 also increased the advance of HIT-T15 cell phase significantly.The results showed that ISL1 promoted proliferation of HIT-T15 cells.

Effects of Haloperidol on Ca2+i Change in HIT T-15 Insulinoma Cells / 대한정신약물학회지

OBJECTIVE: The purpose of this study was to investigate the effects of haloperidol on [Ca2+]i in hamster insulinoma cells (HIT T-15). METHODS: [Ca2+]i levels were measured by calcium imaging techniques, and membrane potential ionic currents were recorded using conventional patch-clamp methods. RESULTS: Haloperidol induced a transient [Ca2+]i increase, which was abolished by the removal of extracellular Ca2+ or pretreatment with Ca2+ channel blockers (nimodipine and mibefradil). Haloperidol depolarized the membrane potential and inhibited the ATP-sensitive K+ (KATP) channels. Sigma receptor agonists, (+)-SKF10047 and ifenprodil, induced a transient [Ca2+]i increase similar to haloperidol. BD1047, a sigma receptor antagonist, completely blocked the [Ca2+]i increase induced by haloperidol. Haloperidol inhibited the KCl-induced [Ca2+]i increase and voltage-dependent Ca2+ currents. Sigma receptor agonists [(+)-SKF10047, ifenprodil] also inhibited the KCl-induced [Ca2+]i increase. CONCLUSION: Our results suggest that haloperidol induces depolarization, which increases [Ca2+]i by voltage-gated Ca2+ currents via the closing of KATP channels. Haloperidol also inhibits KCl-induced [Ca2+]i increases in the same manner. These effects of haloperidol seemed to be mediated by sigma receptors, which might be linked to the pathogenesis of haloperidol-induced diabetes mellitus.

Anti-Apoptotic Effect of Rheum undulatum Water Extract in Pancreatic beta-cell Line, HIT-T15

Sopungsungi-won has been used as a traditional medicine for diabetes and it has been proved to be a potential remedy for type 2 diabetes mellitus. We previously reported that water extract of Sopungsungi-won exhibits anti-diabetic effects both in vivo and in vitro experiments. In the present study, we have chosen to examined anti-apoptotic effect of Rheum undulatum, which is the main component of Sopungsungi-won, on pancreatic beta-cells, HIT-T15, against hydrogen peroxide (H2O2). oxidative stress. To investigate the anti-apoptotic effect of Rheum undulatum water extract (RUWE) against H2O2-induced apoptosis in pancreatic beta-cell line of hamster, HIT-T15, MTT assay, DAPI staining, TUNEL assay, RT-PCR and caspase-3 enzyme assay were performed. The morphological analysis demonstrated that cells treated with H2O2 exhibited classical apoptotic features, while such changes was reduced in cells pre-treated with RUWE. In addition, RUWE pre-treated cells prior to H2O2 treatment induced increase of levels of bcl-2 expression and decrease of caspase-3 enzyme activity compared to cells treated with H2O2 only. These results provide the possibility of usage of RU in patients with progressively deteriorated diabetes.