Double Regulation of Supplement-Detoxification on Diabetic Atherosclerosis by Inhibiting Excessive Autophagy

Fu Xianzhao; Jiang Xiaofeng; Chen Jiajun; Shen Yaya

doi:doi:10.11648/j.wjph.20230801.13

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Double Regulation of Supplement-Detoxification on Diabetic Atherosclerosis by Inhibiting Excessive Autophagy

Fu Xianzhao, Jiang Xiaofeng, Chen Jiajun, Shen Yaya

Published in World Journal of Public Health (Volume 8, Issue 1)

Received: 9 January 2023 Accepted: 6 February 2023 Published: 9 February 2023

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Abstract

Objecive To explore the mechanism of Huoxue Jiedu Jiangtang recipe (HJJR) in regulating the hyperactivation of endoplasmic reticulum stress (ERS) autophagy PERK-eIF2a-LC3 pathway, and reveal its prevention for diabetic atherosclerosis. Methods First, the rats were injected with streptozotocin intraperitoneally to make the diabetic models, and then the aortic balloon injury combined with high-fat feeding were used to make the models of atherosclerosis who were randomly divided into model group, western medicine group (Gliquidone + Benazepril), low-dose HJJR group (HJJR₁), high-dose HJJR group (HJJR₂), and accepted corresponding drugs for 8 weeks respectively. Another blank group was used as control. The changes of serum glycosylated hemoglobin (GHb), homocysteine (Hcy) and angiotensinII (Ang1I) were compared. HE staining was used to detect aortic pathology. The mRNA transcription of PRK-like endoplasmic reticulum kinase (PERK), eucaryotic translation initation factor 2α (eIF2α) and CCAAT / Enhance-Binding Protein Homologous Protein (CHOP) were tested by reverse- transcription polymerase chain reaction (RT-PCR). Western blot were used to detect the expression of autophagy activating protein ATG6 (Beclin-1), autophagy protein microtubule-associated protein light chain LC3-1, LC3-II and LC3-II/LC3-I. Results Compared with the model group, after the drug intervention, the aortic tissue injury in each drug group were reduced, and the improvement in the Chinese medicine group was significantly better than that of the western medicine group (P < 0.05). All treatment groups could significantly lowed the levels of serum GHb, Hcy, and Ang1I (P < 0.05), could down regulate the transcription level of PERK, eIF2α and CHOP mRNA (P < 0.05); and decreased the amount of Beclin 1, LC3-II and LC3-II/LC3-1 autophagy protein in aortic cells (P < 0.05). The effect of HJJF group was better, and it was more significant with the increase of HJJF dose. Conclusion HJJR can protect arteries by inhibiting ERS caused by metabolic disorder in diabetes, correcting the homeostasis affecting ER, reducing the overreaction of PERK-eIF2-LC3, and alleviating autophagy effect.

Published in	World Journal of Public Health (Volume 8, Issue 1)
DOI	10.11648/j.wjph.20230801.13
Page(s)	15-22
Creative Commons	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

Diabetes Mellitus, Atherosclerosis, Huoxue Jiedu Jiangtang Recipe, Endoplasmic Reticulum Stress, Autophagy

References

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[4]	Fu Xianzhao, Xu Jing, Li Chunyan, et al. Efects of Huoxue Jiedu Jiang tang formulation on the balance between pro-and anti-inf lammatory cytokines in non-revascularization patients with diabetic acute coronary syndrome [J]. ChinJ TCM WM Crit Care, 2016, 23 (1): 6-10.
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APA Style

Fu Xianzhao, Jiang Xiaofeng, Chen Jiajun, Shen Yaya. (2023). Double Regulation of Supplement-Detoxification on Diabetic Atherosclerosis by Inhibiting Excessive Autophagy. World Journal of Public Health, 8(1), 15-22. https://doi.org/10.11648/j.wjph.20230801.13

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ACS Style

Fu Xianzhao; Jiang Xiaofeng; Chen Jiajun; Shen Yaya. Double Regulation of Supplement-Detoxification on Diabetic Atherosclerosis by Inhibiting Excessive Autophagy. World J. Public Health 2023, 8(1), 15-22. doi: 10.11648/j.wjph.20230801.13

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AMA Style

Fu Xianzhao, Jiang Xiaofeng, Chen Jiajun, Shen Yaya. Double Regulation of Supplement-Detoxification on Diabetic Atherosclerosis by Inhibiting Excessive Autophagy. World J Public Health. 2023;8(1):15-22. doi: 10.11648/j.wjph.20230801.13

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@article{10.11648/j.wjph.20230801.13,
  author = {Fu Xianzhao and Jiang Xiaofeng and Chen Jiajun and Shen Yaya},
  title = {Double Regulation of Supplement-Detoxification on Diabetic Atherosclerosis by Inhibiting Excessive Autophagy},
  journal = {World Journal of Public Health},
  volume = {8},
  number = {1},
  pages = {15-22},
  doi = {10.11648/j.wjph.20230801.13},
  url = {https://doi.org/10.11648/j.wjph.20230801.13},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.wjph.20230801.13},
  abstract = {Objecive To explore the mechanism of Huoxue Jiedu Jiangtang recipe (HJJR) in regulating the hyperactivation of endoplasmic reticulum stress (ERS) autophagy PERK-eIF2a-LC3 pathway, and reveal its prevention for diabetic atherosclerosis. Methods First, the rats were injected with streptozotocin intraperitoneally to make the diabetic models, and then the aortic balloon injury combined with high-fat feeding were used to make the models of atherosclerosis who were randomly divided into model group, western medicine group (Gliquidone + Benazepril), low-dose HJJR group (HJJR1), high-dose HJJR group (HJJR2), and accepted corresponding drugs for 8 weeks respectively. Another blank group was used as control. The changes of serum glycosylated hemoglobin (GHb), homocysteine (Hcy) and angiotensinII (Ang1I) were compared. HE staining was used to detect aortic pathology. The mRNA transcription of PRK-like endoplasmic reticulum kinase (PERK), eucaryotic translation initation factor 2α (eIF2α) and CCAAT / Enhance-Binding Protein Homologous Protein (CHOP) were tested by reverse- transcription polymerase chain reaction (RT-PCR). Western blot were used to detect the expression of autophagy activating protein ATG6 (Beclin-1), autophagy protein microtubule-associated protein light chain LC3-1, LC3-II and LC3-II/LC3-I. Results Compared with the model group, after the drug intervention, the aortic tissue injury in each drug group were reduced, and the improvement in the Chinese medicine group was significantly better than that of the western medicine group (P Conclusion HJJR can protect arteries by inhibiting ERS caused by metabolic disorder in diabetes, correcting the homeostasis affecting ER, reducing the overreaction of PERK-eIF2-LC3, and alleviating autophagy effect.},
 year = {2023}
}

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TY  - JOUR
T1  - Double Regulation of Supplement-Detoxification on Diabetic Atherosclerosis by Inhibiting Excessive Autophagy
AU  - Fu Xianzhao
AU  - Jiang Xiaofeng
AU  - Chen Jiajun
AU  - Shen Yaya
Y1  - 2023/02/09
PY  - 2023
N1  - https://doi.org/10.11648/j.wjph.20230801.13
DO  - 10.11648/j.wjph.20230801.13
T2  - World Journal of Public Health
JF  - World Journal of Public Health
JO  - World Journal of Public Health
SP  - 15
EP  - 22
PB  - Science Publishing Group
SN  - 2637-6059
UR  - https://doi.org/10.11648/j.wjph.20230801.13
AB  - Objecive To explore the mechanism of Huoxue Jiedu Jiangtang recipe (HJJR) in regulating the hyperactivation of endoplasmic reticulum stress (ERS) autophagy PERK-eIF2a-LC3 pathway, and reveal its prevention for diabetic atherosclerosis. Methods First, the rats were injected with streptozotocin intraperitoneally to make the diabetic models, and then the aortic balloon injury combined with high-fat feeding were used to make the models of atherosclerosis who were randomly divided into model group, western medicine group (Gliquidone + Benazepril), low-dose HJJR group (HJJR1), high-dose HJJR group (HJJR2), and accepted corresponding drugs for 8 weeks respectively. Another blank group was used as control. The changes of serum glycosylated hemoglobin (GHb), homocysteine (Hcy) and angiotensinII (Ang1I) were compared. HE staining was used to detect aortic pathology. The mRNA transcription of PRK-like endoplasmic reticulum kinase (PERK), eucaryotic translation initation factor 2α (eIF2α) and CCAAT / Enhance-Binding Protein Homologous Protein (CHOP) were tested by reverse- transcription polymerase chain reaction (RT-PCR). Western blot were used to detect the expression of autophagy activating protein ATG6 (Beclin-1), autophagy protein microtubule-associated protein light chain LC3-1, LC3-II and LC3-II/LC3-I. Results Compared with the model group, after the drug intervention, the aortic tissue injury in each drug group were reduced, and the improvement in the Chinese medicine group was significantly better than that of the western medicine group (P Conclusion HJJR can protect arteries by inhibiting ERS caused by metabolic disorder in diabetes, correcting the homeostasis affecting ER, reducing the overreaction of PERK-eIF2-LC3, and alleviating autophagy effect.
VL  - 8
IS  - 1
ER  -

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Author Information

Fu Xianzhao

The Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, China
Jiang Xiaofeng

The Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, China
Chen Jiajun

The Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, China
Shen Yaya

The Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, China

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APA Style

Fu Xianzhao, Jiang Xiaofeng, Chen Jiajun, Shen Yaya. (2023). Double Regulation of Supplement-Detoxification on Diabetic Atherosclerosis by Inhibiting Excessive Autophagy. World Journal of Public Health, 8(1), 15-22. https://doi.org/10.11648/j.wjph.20230801.13

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ACS Style

Fu Xianzhao; Jiang Xiaofeng; Chen Jiajun; Shen Yaya. Double Regulation of Supplement-Detoxification on Diabetic Atherosclerosis by Inhibiting Excessive Autophagy. World J. Public Health 2023, 8(1), 15-22. doi: 10.11648/j.wjph.20230801.13

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AMA Style

Fu Xianzhao, Jiang Xiaofeng, Chen Jiajun, Shen Yaya. Double Regulation of Supplement-Detoxification on Diabetic Atherosclerosis by Inhibiting Excessive Autophagy. World J Public Health. 2023;8(1):15-22. doi: 10.11648/j.wjph.20230801.13

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@article{10.11648/j.wjph.20230801.13,
  author = {Fu Xianzhao and Jiang Xiaofeng and Chen Jiajun and Shen Yaya},
  title = {Double Regulation of Supplement-Detoxification on Diabetic Atherosclerosis by Inhibiting Excessive Autophagy},
  journal = {World Journal of Public Health},
  volume = {8},
  number = {1},
  pages = {15-22},
  doi = {10.11648/j.wjph.20230801.13},
  url = {https://doi.org/10.11648/j.wjph.20230801.13},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.wjph.20230801.13},
  abstract = {Objecive To explore the mechanism of Huoxue Jiedu Jiangtang recipe (HJJR) in regulating the hyperactivation of endoplasmic reticulum stress (ERS) autophagy PERK-eIF2a-LC3 pathway, and reveal its prevention for diabetic atherosclerosis. Methods First, the rats were injected with streptozotocin intraperitoneally to make the diabetic models, and then the aortic balloon injury combined with high-fat feeding were used to make the models of atherosclerosis who were randomly divided into model group, western medicine group (Gliquidone + Benazepril), low-dose HJJR group (HJJR1), high-dose HJJR group (HJJR2), and accepted corresponding drugs for 8 weeks respectively. Another blank group was used as control. The changes of serum glycosylated hemoglobin (GHb), homocysteine (Hcy) and angiotensinII (Ang1I) were compared. HE staining was used to detect aortic pathology. The mRNA transcription of PRK-like endoplasmic reticulum kinase (PERK), eucaryotic translation initation factor 2α (eIF2α) and CCAAT / Enhance-Binding Protein Homologous Protein (CHOP) were tested by reverse- transcription polymerase chain reaction (RT-PCR). Western blot were used to detect the expression of autophagy activating protein ATG6 (Beclin-1), autophagy protein microtubule-associated protein light chain LC3-1, LC3-II and LC3-II/LC3-I. Results Compared with the model group, after the drug intervention, the aortic tissue injury in each drug group were reduced, and the improvement in the Chinese medicine group was significantly better than that of the western medicine group (P Conclusion HJJR can protect arteries by inhibiting ERS caused by metabolic disorder in diabetes, correcting the homeostasis affecting ER, reducing the overreaction of PERK-eIF2-LC3, and alleviating autophagy effect.},
 year = {2023}
}

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TY  - JOUR
T1  - Double Regulation of Supplement-Detoxification on Diabetic Atherosclerosis by Inhibiting Excessive Autophagy
AU  - Fu Xianzhao
AU  - Jiang Xiaofeng
AU  - Chen Jiajun
AU  - Shen Yaya
Y1  - 2023/02/09
PY  - 2023
N1  - https://doi.org/10.11648/j.wjph.20230801.13
DO  - 10.11648/j.wjph.20230801.13
T2  - World Journal of Public Health
JF  - World Journal of Public Health
JO  - World Journal of Public Health
SP  - 15
EP  - 22
PB  - Science Publishing Group
SN  - 2637-6059
UR  - https://doi.org/10.11648/j.wjph.20230801.13
AB  - Objecive To explore the mechanism of Huoxue Jiedu Jiangtang recipe (HJJR) in regulating the hyperactivation of endoplasmic reticulum stress (ERS) autophagy PERK-eIF2a-LC3 pathway, and reveal its prevention for diabetic atherosclerosis. Methods First, the rats were injected with streptozotocin intraperitoneally to make the diabetic models, and then the aortic balloon injury combined with high-fat feeding were used to make the models of atherosclerosis who were randomly divided into model group, western medicine group (Gliquidone + Benazepril), low-dose HJJR group (HJJR1), high-dose HJJR group (HJJR2), and accepted corresponding drugs for 8 weeks respectively. Another blank group was used as control. The changes of serum glycosylated hemoglobin (GHb), homocysteine (Hcy) and angiotensinII (Ang1I) were compared. HE staining was used to detect aortic pathology. The mRNA transcription of PRK-like endoplasmic reticulum kinase (PERK), eucaryotic translation initation factor 2α (eIF2α) and CCAAT / Enhance-Binding Protein Homologous Protein (CHOP) were tested by reverse- transcription polymerase chain reaction (RT-PCR). Western blot were used to detect the expression of autophagy activating protein ATG6 (Beclin-1), autophagy protein microtubule-associated protein light chain LC3-1, LC3-II and LC3-II/LC3-I. Results Compared with the model group, after the drug intervention, the aortic tissue injury in each drug group were reduced, and the improvement in the Chinese medicine group was significantly better than that of the western medicine group (P Conclusion HJJR can protect arteries by inhibiting ERS caused by metabolic disorder in diabetes, correcting the homeostasis affecting ER, reducing the overreaction of PERK-eIF2-LC3, and alleviating autophagy effect.
VL  - 8
IS  - 1
ER  -

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