Objecive: To study the effects of Huoxue Jiedu Jiangtang formulation (HJJF) on endoplasmic reticulum stress (ERS) coupled inflammatory response From the molecular mechanism in diabetic vascular disease. Methods: Type 2 diabetes were established in male SD rats by feeding high lipid diet and injection of streptozotocin. after T2DM models established successfully, the rats were divided into model group, low-dose HJJF group (HJJF 1 ), high-dose HJJF group (HJJF 2 ), and Western medicine group (Gliquidone+Benazepril), and accepted corresponding drugs for 8 weeks respectively. Another normal group were used as control group, fed with normal diet, no drug intervention. The levels of fasting blood glucose (FBG), serum superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), IL-6 and TNF-α were tested. The ERS signaling molecules glucose-regulated protein 78 (GRP78) and c-Jun N-terminal kinases (JNK) mRNA transcription level in thoracic aorta vessel were determined by reverse-transcription polymerase chain reaction (RT-PCR). Results: Compared with model group, After drugs intervention, all administered groups could significantly decrease FPG (P<0.05), elevate SOD and GSH-Px (P<0.05); all could reduce levels of TC, TG, LDL-C, IL-6 and TNF-α (P<0.05), and raise HDL-C (P<0.05); all could depress the transcription levels of GRP78 and JNK mRNA (P<0.05). With increasing dose, the HJJF effect is more significant (P<0.05). Conclusion: HJJF could improve insulin resistance, correct lipid metabolism disorders, and enhance the antioxidative ability, inhibit the response of ERS coupled inflammatory, showing the multi-target treatment characteristics of Traditional Chinese Medicine.

To explore the mechanism of Huoxue Jiedu Jiangtang Recipe (HJJR) in alleviating endoplasmic reticulum stress (ERS) -inflammation, inhibiting ERS apoptotic bypass of CHOP and alleviating diabetic atherosclerosis (AS). Diabetic AS rats were duplicated by feeding of high lipid diet and intraperitoneal injection of streptozotocin. After diabetes modeled successfully, the rats were randomly divided into model group, low-dose HJJR group (HJJR 1 ), high-dose HJJR group (HJJR 2 ) and western medicine group (Gliquidone+ Benazepril), and accepted corresponding drugs for 2 months respectively. The same batch of rats were taken as normal control group and fed with common diet. The levels of glycosylated hemoglobin (GHb), blood lipid, fasting serum insulin (FINS) and insulin resistance index (IRI) were measured in each group. The contents of inflammatory factors TNF-α and IL-6 were detected by immunohistochemistry. The mRNA transcription of GRP78 and caspase-12 were tested by reverse-transcription polymerase chain reaction (RT-PCR). The apoptotic level of aortic cells was checked by TUNEL. Compared with the model group, all drug groups could significantly reduce GHb, IRI, TG and LDL-C (P<0.05), increase FINS and HDL-C (P<0.05), down-regulate transcription of CHOP and GRP78 (P<0.05), reduce inflammatory factors TNF-a, IL-6, and decreased aortic apoptosis index (AI) (P<0.05). Compared with the western medicine group, the effect of HJJR2 group was more significant (P<0.05). HJJR could alleviate insulin resistance, correct lipid metabolism disorder, depress endoplasmic reticulum stress-induced inflammatory reaction, and inhibit endoplasmic reticulum stress-induced apoptotic bypass of CHOP in arterial cells. The therapeutic effect is dose dependent.

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Objective To explore the therapeutic molecular mechanism of Jiang Tang Shu Xin (JTSX) recipe with"invigorating Qi, nourishing Yin, activating blood circulation and detoxifying" in improving insulin resistance, inhibiting apoptotic bypass of endoplasmic reticulum stress (ERS) CCAAT enhance-binding protein homologous protein (CHOP), improving diabetic myocardial remodeling in SD diabetic rats. Methods SD rats were used to establish diabetes mellitus models, and after modeled successfully, were randomly divided into model group, western medicine group (Gliquidone+ Benazepril), low-dose JTSX group (JTSX 1), high-dose JTSX group (JTSX 2), and accepted corresponding drugs for 2 months respectively, taking the same batch of rats as normal control. After drugs administration finishing, blood lipid were measured by automatic biochemical analyzer, fasting serum insulin (FINS) and glycosylated hemoglobin (GHb) were measured by enzyme-linked immunosorbent assay (ELISA), insulin resistance index (IRI) was calculated. Masson staining was used to detect the expression of myocardial collagen fibers, immunohistochemistry to test the expression of myocardial nuclear factor-kB (NF-kB), tumor necrosis factor-alpha (TNF-α), TUNEL to check the apoptotic level of myocardial cells, RT-PCR to detect the transcription level of ERS molecules glucose regulated protein 78 (GRP78) and CHOP. Results Compared with the model group, the treatment groups could significantly reduce TG, LDL-C, GHb and IRI (P<0.05), increase FINS and HDL-C (P<0.05), decrease inflammatory factors NF-kB and TNF-α (P<0.05), down-regulate transcription of CHOP and GRP78 (P<0.05), and reduce cardiomyocyte apoptosis index (AI) (P<0.05); compared with the western medicine group, JTSX2 had more significant effect (P<0.05). Conclusion JTSX can inhibit insulin resistance, correct lipid metabolism disorder, restrain ERS-induced inflammatory reaction, suppress ERS-initiated apoptotic bypass of CHOP, and improve myocardial remodeling, with dose-dependent.