四君子颗粒对大鼠糖尿病前期的改善作用

目的探讨四君子颗粒对大鼠糖尿病前期的改善作用。方法采用高糖高脂饮食建立糖尿病前期大鼠模型,随机分为正常组、模型组、四君子颗粒高、低剂量组(10.50、5.25 g/kg),连续灌胃10周。分别于第2、4、6、8、10周末检测FBG、FINS、GHb水平并计算Homa-IR,第10周末采用TUNEL染色法检测胰岛细胞凋亡水平,Western blot法检测胰腺组织p-PERK、GRP78、ATF4、CHOP蛋白表达。结果糖尿病前期大鼠FBG、GHb、FINS水平及Homa-IR均升高(P<0.01),胰岛中凋亡细胞增多,胰腺组织p-PERK、GRP78、ATF4、CHOP蛋白表达升高(P<0.05,P<0.01)。给予四君子颗粒后,血清FBG、GHb、FINS水平和Homa-IR降低(P<0.05,P<0.01),胰岛细胞凋亡减少,同时,胰腺组织p-PERK、GRP78、ATF4、CHOP蛋白表达下降(P<0.05,P<0.01)。结论四君子颗粒可明显改善大鼠糖尿病前期状态,其机制可能与减轻糖尿病前期大鼠胰岛素抵抗、抑制内质网应激诱导的胰岛细胞凋亡有关。

Effects of Sijunzi Granules on prediabetes in rats

AIM To investigate the effect of Sijunzi Granules on prediabetes improvement in rats.METHODS A prediabetic rat model was established using a high-sugar and high-fat diet feeding. The rats were randomly divided into normal group, model group, high-dose and low-dose Sijunzi Granules groups(10.50, 5.25 g/kg) for 10-week consecutive gavage. FBG, FINS, and GHb levels were detected and Homa-IR was calculated at the end of the 2nd, 4th, 6th, 8th, and 10th weekends, respectively. At the end of the 10th weekend, rats were subjected to detection of apoptosis of pancreatic islet cells by TUNEL staining, and determination of protein expressions of p-PERK, GRP78, ATF4 and CHOP in pancreatic tissues by Western blot.RESULTS In prediabetic, the levels of FBG, GHb, FINS and Homa-IR in rats were increased(P<0.01). There were more apoptotic cells in pancreatic islets of rats, and the expression of p-PERK, GRP78, ATF4, and CHOP proteins in pancreatic tissues was increased(P<0.05, P<0.01). After administration of Sijunzi Granules, serum levels of FBG, GHb, FINS, and Homa-IR were reduced(P<0.05, P<0.01), and islet cell apoptosis was reduced. Meanwhile, reduced expressions of p-PERK, GRP78, ATF4, and CHOP proteins in pancreatic tissues were observable as well(P<0.05, P<0.01).CONCLUSION Sijunzi Granules can significantly improve rats’ pre-diabetic condition, and its relevant mechanism may contribute to the reduction of insulin resistance and inhibition of endoplasmic reticulum-induced islet apoptosis.