Issue |
BIO Web Conf.
Volume 49, 2022
The 3rd International Symposium on Global Physiology 2022 (ISGP 2022)
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Article Number | 03004 | |
Number of page(s) | 7 | |
Section | Human Physiology | |
DOI | https://doi.org/10.1051/bioconf/20224903004 | |
Published online | 05 July 2022 |
Chlorogenic Acid Ameliorates Liver Function in Association with Bax Downregulation, P53 Downregulation and Bcl-2 Upregulation in Diabetic Wistar Rat
1 Master in Biomedical Science Program, Faculty of Medicine, Public Health, and Nursing, Universitas GadjahMada, Yogyakarta
2 Department of Physiology, Faculty of Medicine, Public Health, and Nursing, Universitas Gadjah Mada, Yogyakarta
3 Department of Anatomic Pathology, Faculty of Medicine, Public Health, and Nursing, Universitas Gadjah Mada, Yogyakarta
4 Department of Anatomy, Faculty of Medicine, Public Health, and Nursing, Universitas Gadjah Mada, Yogyakarta
* Corresponding author: mayangsetyaningsih@mail.ugm.ac.id
Hyperglycemia in Diabetes mellitus (DM) induces oxidative stress and mitochondrial disruptions in the liver, thereby triggering apoptosis through Bcl-2 family signaling. Excessive apoptosis leads to liver dysfunction. Chlorogenic acid (CGA) was elucidated in this study in preventing liver dysfunction as a progression of DM. The diabetic model was conducted in Wistar rats, divided into six groups. Blood examinations were done to measure the levels of blood glucose, SGOT, and SGPT. The liver was harvested for analysis of SOD2, Bax, and Bcl-2 mRNA. A paraffin section was used for p53 immunostaining. Liver dysfunction occurred in the DM 2 months group indicated by higher levels of SGPT and SGOT, higher expression of Bax, and lower expression of Bcl-2 compared to the control group. Giving CGA 12.5 mg/kgBW ameliorated blood glucose and liver enzyme levels, which were associated with lower expression of Bax, lower signaling of p53, and higher expression of Bcl-2 compared to DM 2 months group. Administration of CGA did not affect SOD2 expression in diabetic rats. CGA may attenuate liver dysfunction in diabetic rats through downregulation of Bax and p53, and upregulation of Bcl-2 signaling.
© The Authors, published by EDP Sciences, 2022
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