Science Journal of Public Health

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

Received: Oct. 28, 2019    Accepted:     Published: Jan. 07, 2020
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Abstract

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 (JTSX1), high-dose JTSX group (JTSX2), 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.

DOI 10.11648/j.sjph.20190706.17
Published in Science Journal of Public Health ( Volume 7, Issue 6, November 2019 )
Page(s) 225-231
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This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2024. Published by Science Publishing Group

Keywords

Endoplasmic Reticulum Stress, Apoptosis, CCAAT Enhance-Binding Protein Homologous Protein, Myocardial Remodeling, Jiang Tang Shu Xin Recipe

References
[1] Wu QQ, Xiao Y, Yuan Y, et a1. Mechanisms contributing to cardiac remodelling [J]. Clin Sci (Lond), 2017, 24; 131 (18): 2319-2345.
[2] Othman AI, El-Sawi MR El-Missiry MA, et al. Epigallocatechin-3-gallate protects against diabetic cardiomyopathy through modulating the cardiometabolic risk factors, oxidative stress, inflammation, cell death and fibrosis in streptozotocin-nicotinamide-induced diabetic rats. Biomed Pharmacother [J]. 2017, 94: 362-373.
[3] Zhang B, Zhang P, Tan Y, et al. C1q-TNF-related protein-3 attenuates pressure overload-induced cardiac hypertrophy by suppressing the p38/CREB pathway and p38-induced ER stress. Cell Death Dis. 2019, 10 (7): 520. doi: 10.1038/s41419-019-1749-0.
[4] Fu Xianzhao, Huang Zhenfeng, Huang Wenhua, et al. Review and Prospect of the Preventive Effect of “Supplementing Qi and Nourishing Yin, Activating Blood Circulation and Detoxifying” on Diabetes Mellitus Complicated with Acute Coronary Syndrome. American Journal of Clinical and Experimental Medicine. 2018, 6 (4): 87-93.
[5] FU Xian-zhao, HUANG Yue-feng, WANG Qing-li, et a1. Effect of Jiangtang Shuxin decoction on diabetic patients with chronic heart failure: a prospective randomized controlled study [J]. Chin J TCM WM Crit Care, 2017, 24 (2): 123-126.
[6] Fu Xianzhao, Feng Xueping, Huang Wenhua, et al. Effect of Jiangtang Shuxin recipe on endoplasmic reticulum stress c-JNK apoptosis pathway in diabetic myocardium. CHINESE ARCHIVES OF TRADITIONAL CHINESE MEDICINE, 2018, 36 (10): 2423-2427.
[7] Fu Xianzhao, Feng Xueping, Qiu HaiXian, et al. Effect of Jiangtang Shuxin recipe on diabetic cardiomyocyte endoplasmic reticulum stress caspase-12 apoptosis pathway and heart function. CHINESE ARCHIVES OF TRADITIONAL CHINESE MEDICINE, 2019, 37 (9): 2068-2073.
[8] Wu J, Pan W, Wang C, et al. H2S attenuates endoplasmic reticulum stress in hypoxia-induced pulmonary artery hypertension. Biosci Rep. 2019 Jul 8; 39 (7). pii: BSR20190304.
[9] Lin R, Su Z, Tan X, et al. Effect of Endoplasmic Reticulum Stress and Autophagy in the Regulation of Post-infarct Cardiac Repair. Arch Med Res. 2018 Nov; 49 (8): 576-582.
[10] Li J, Yue G, Ma W, et al. Ufm1-Specific Ligase Ufl1Regulates Endoplasmic Reticulum Homeostasis and Protects Against Heart Failure. Circ Heart Fail. 2018 Oct; 11 (10): e004917.
[11] Hu H, Wang C, Jin Y, et al. Catalpol Inhibits Homocysteine-induced Oxidation and Inflammation via Inhibiting Nox4/NF-κB and GRP78/PERK Pathways in Human Aorta Endothelial Cells. Inflammation. 2019 Feb; 42 (1): 64-80.
[12] Chen Y, Zhang B, Cao S, et al. GanDouLing combined with Penicillamine improves cerebrovascular injury via PERK/eIF2α/CHOP endoplasmic reticulum stress pathway in the mouse model of Wilson's disease. Biosci Rep. 2018 Sep 19; 38 (5). pii: BSR20180800.
[13] Oyadomari S, Mori M. Roles of CHOP/GADDI53 in endoplasmic reticulum stress [J]. Cell Death Differ, 2004, 11: 381-389.
[14] Liao Y, Chen K, Dong X, et al. Berberine inhibits cardiac remodeling of heart failure after myocardial infarction by reducing myocardial cell apoptosis in rats. Exp Ther Med. 2018, 16 (3): 2499-2505.
[15] Yang L, Zhao D, Ren J, et al. Endoplasmic reticulum stress and protein quality control in diabetic cardiomyopathy. Biochim Biophys Acta, 2015, 1852 (2): 209-18.
[16] Darnel P, Miles J D B, Chengxue Q, et al. Phosphoinositide 3-Kinase (p110α) Gene Delivery Limits Diabetes-induced Cardiac NADPH Oxidase and Cardiomyopathy in a Mouse Model with Established Diastolic Dysfunction. Clinical Science, 2017, 131 (12): 1345.
[17] Paras K, Mishra, Wei Ying. Diabetic Cardiomyopathy: An immunometabolic Perspective. frontiers in Endocrinology, doi: 10.3389/fendo.2017.00072.
[18] Wang WK, Lu QH, Wang X, et al. Ulinastatin attenuates diabetes-induced cardiac dysfunction by the inhibition of inflammation and apoptosis. Exp Ther Med, 2017, 14 (3): 2497-2504.
[19] Chang P, Zhang M, Zhang X, et a1. B-type natriuretic peptide attenuates endoplasmic reticulum stress in H9c2 cardiomyocytes underwent hypoxia/reoxygenation injury under high glucose/ high fat conditions. Peptides, 2018 Apr 22. pii: S0196-9781(18)30090-1. doi: 10.1016/j.
[20] FU Xian-zhao, XU Jing, HUANG WenHua, et a1. Strategy of Stasis-resolving and Detoxification on Diabetic Coronary Heart Disease [J]. JETCM, 2014, 23 (11): 2024-2027.
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    Fu Xianzhao, Huang Guangming, Li Chunyan, Huang Wenhua, Qiu Haixian, et al. (2020). Inhibition of Jiang Tang Shu Xin (JTSX) Recipe in Endoplasmic Reticulum Stress CHOP Pathway and Improving Myocardial Remodeling in SD Diabetic Rats. Science Journal of Public Health, 7(6), 225-231. https://doi.org/10.11648/j.sjph.20190706.17

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    ACS Style

    Fu Xianzhao; Huang Guangming; Li Chunyan; Huang Wenhua; Qiu Haixian, et al. Inhibition of Jiang Tang Shu Xin (JTSX) Recipe in Endoplasmic Reticulum Stress CHOP Pathway and Improving Myocardial Remodeling in SD Diabetic Rats. Sci. J. Public Health 2020, 7(6), 225-231. doi: 10.11648/j.sjph.20190706.17

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    AMA Style

    Fu Xianzhao, Huang Guangming, Li Chunyan, Huang Wenhua, Qiu Haixian, et al. Inhibition of Jiang Tang Shu Xin (JTSX) Recipe in Endoplasmic Reticulum Stress CHOP Pathway and Improving Myocardial Remodeling in SD Diabetic Rats. Sci J Public Health. 2020;7(6):225-231. doi: 10.11648/j.sjph.20190706.17

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  • @article{10.11648/j.sjph.20190706.17,
      author = {Fu Xianzhao and Huang Guangming and Li Chunyan and Huang Wenhua and Qiu Haixian and Qiu Siyuan and Bi Honghan and Cao Qiuxia and Lu Mian},
      title = {Inhibition of Jiang Tang Shu Xin (JTSX) Recipe in Endoplasmic Reticulum Stress CHOP Pathway and Improving Myocardial Remodeling in SD Diabetic Rats},
      journal = {Science Journal of Public Health},
      volume = {7},
      number = {6},
      pages = {225-231},
      doi = {10.11648/j.sjph.20190706.17},
      url = {https://doi.org/10.11648/j.sjph.20190706.17},
      eprint = {https://download.sciencepg.com/pdf/10.11648.j.sjph.20190706.17},
      abstract = {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 (JTSX1), high-dose JTSX group (JTSX2), 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 (PConclusion 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.},
     year = {2020}
    }
    

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  • TY  - JOUR
    T1  - Inhibition of Jiang Tang Shu Xin (JTSX) Recipe in Endoplasmic Reticulum Stress CHOP Pathway and Improving Myocardial Remodeling in SD Diabetic Rats
    AU  - Fu Xianzhao
    AU  - Huang Guangming
    AU  - Li Chunyan
    AU  - Huang Wenhua
    AU  - Qiu Haixian
    AU  - Qiu Siyuan
    AU  - Bi Honghan
    AU  - Cao Qiuxia
    AU  - Lu Mian
    Y1  - 2020/01/07
    PY  - 2020
    N1  - https://doi.org/10.11648/j.sjph.20190706.17
    DO  - 10.11648/j.sjph.20190706.17
    T2  - Science Journal of Public Health
    JF  - Science Journal of Public Health
    JO  - Science Journal of Public Health
    SP  - 225
    EP  - 231
    PB  - Science Publishing Group
    SN  - 2328-7950
    UR  - https://doi.org/10.11648/j.sjph.20190706.17
    AB  - 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 (JTSX1), high-dose JTSX group (JTSX2), 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 (PConclusion 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.
    VL  - 7
    IS  - 6
    ER  - 

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Author Information
  • Clinic Medical College, Youjiang Medical National College, Baise, China

  • Clinic Medical College, Youjiang Medical National College, Baise, China

  • Clinic Medical College, Youjiang Medical National College, Baise, China

  • Clinic Medical College, Youjiang Medical National College, Baise, China

  • Clinic Medical College, Youjiang Medical National College, Baise, China

  • Clinic Medical College, Youjiang Medical National College, Baise, China

  • Clinic Medical College, Youjiang Medical National College, Baise, China

  • Clinic Medical College, Youjiang Medical National College, Baise, China

  • Clinic Medical College, Youjiang Medical National College, Baise, China

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