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Original Research Article | OPEN ACCESS

Pachymic acid protects against kidney injury in mice with diabetic nephropathy by inhibiting the PI3K/AKT pathway

Weihao Li1,2 , Chong Wang3, Mingming Zhang4, Yingze Yuan5, Zhiping Zhang2, Xiaomei Liu2, Feifei Zhang2, Yuefeng Wu1

1Key Laboratory of Animal Physiology, Biochemistry and Molecular Biology of Hebei Province, College of Life Sciences, Hebei Normal University, Shijiazhuang, Hebei Province 050024, China,; 2Special Clinical Laboratory, Second Hospital of Hebei Medical University, Hebei Province 050000, China; 3Department of Laboratory Medicine, East Branch of Second Hospital of Hebei Medical University, Shijiazhuang, Hebei Province 050000, China; 4Clinical Laboratory, Hebei General Hospital, Shijiazhuang, Hebei Province 050001, China; 5Department of Laboratory Medicine, Jizhong Energy Xingtai MIG General Hospital, Xingtai, Hebei Province 054000, China.

For correspondence:-  Weihao Li   Email: wuyuefeng@hebtu.edu.cn   Tel:+8631166636290

Accepted: 29 November 2021        Published: 30 December 2021

Citation: Li W, Wang C, Zhang M, Yuan Y, Zhang Z, Liu X, et al. Pachymic acid protects against kidney injury in mice with diabetic nephropathy by inhibiting the PI3K/AKT pathway. Trop J Pharm Res 2021; 20(12):2539-2544 doi: 10.4314/tjpr.v20i12.12

© 2021 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To investigate the effect of pachymic acid (PA) on diabetic nephropathy (DN).
Methods: C57BL/6J mice were divided into three groups: control group, DN model group, and PA group. In the DN model and PA groups, the mice were injected intraperitoneally with streptozotocin (STZ) on five consecutive days to induce DN. In the control group, the mice were injected with saline. Then, mice in the PA group were treated with 5 mg/100 g PA for four consecutive weeks. Weight and fasting blood glucose were measured. The pathological condition of kidney tissue was examined by hematoxylin/eosin staining. Serum creatinine (Scr), urea nitrogen (BUN), urine protein (U-Pro), malondialdehyde (MDA), and superoxide dismutase (SOD) levels in kidney tissues were measured by enzyme immunosorbent assay (ELISA). Protein expression of AKT, PI3K, p-AKT, and p-PI3K in kidney tissues was evaluated by western blot.
Results: Compared with the control group, mice in the DN model group weighed less; had a higher degree of kidney tissue damage; higher fasting blood glucose, Scr, BUN, U-Pro, MDA, p-AKT, and p-PI3K levels; and lower SOD activity. Compared with the DN model group, the PA group showed improvements in weight and kidney damage; had lower fasting blood glucose, Scr, BUN, U-Pro, p-AK, and p-PI3K levels; and higher SOD activity.
Conclusion: PA treatment improves the renal function of DN mice and inhibits oxidative stress, probably by suppressing the PI3K/AKT pathway. These findings suggest that PA has potentials as a treatment for DN.

Keywords: Pachymic acid, Diabetic nephropathy, Oxidative stress, PI3K/AKT signaling pathway, Kidney injury

Impact Factor
Thompson Reuters (ISI): 0.6 (2023)
H-5 index (Google Scholar): 49 (2023)

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