Inhibition of Jiang Tang Shu Xin (JTSX) Recipe in Endoplasmic Reticulum Stress CHOP Pathway and Improving Myocardial Remodeling in SD Diabetic Rats

Fu Xianzhao, Huang Guangming, Li Chunyan, Huang Wenhua, Qiu Haixian, Qiu Siyuan, Bi Honghan, Cao Qiuxia, Lu Mian
<span title="">2019</span> <i title="Science Publishing Group"> <a target="_blank" rel="noopener" href="https://fatcat.wiki/container/ih34hv53hfaphekwrnywayy4yy" style="color: black;">Science Journal of Public Health</a> </i> &nbsp;
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
more &raquo; ... domly 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.
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