Evidence map›Paper›PMID 41020010›Full record

ArticleFrontiers in pharmacology2025

Exploration of the renoprotective effect of Yi-Shen-Hua-Shi granules on db/db mice and the mechanism of podocyte apoptosis based on the GRP78/CHOP signaling pathway.

Yanmo Cai, Yunhua Liu, Sitong Wang, Ge Jin, Kaidong Zhou, Xin Zhou, Xinxue Zhang, Min Zhang, Zongjiang Zhao

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Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

9 authors.

Yanmo Cai *International Acupuncture and Moxibustion Innovation Institute, School of Acupuncture-Moxibustion and Tuina, Beijing University of Chinese Medicine, Beijing, China.
Yunhua Liu *International Acupuncture and Moxibustion Innovation Institute, School of Acupuncture-Moxibustion and Tuina, Beijing University of Chinese Medicine, Beijing, China.
Sitong WangBeijing University of Chinese Medicine, Beijing, China.
Ge JinBeijing University of Chinese Medicine, Beijing, China.
Kaidong ZhouBeijing University of Chinese Medicine, Beijing, China.
Xin ZhouBeijing University of Chinese Medicine, Beijing, China.
Xinxue ZhangBeijing University of Chinese Medicine, Beijing, China.
Min ZhangBeijing Chaoyang Hospital, Capital Medical University, Beijing, China.
Zongjiang ZhaoBeijing University of Chinese Medicine, Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: Yi-Shen-Hua-Shi (YSHS) granules are a widely utilized Chinese medicine formula for treating diabetic kidney disease (DKD). Although their effectiveness in treating DKD is established, the precise regulatory mechanism remains unclear. We aimed to explore the potential targets and mechanisms of action of YSHS in delaying DKD progression through network pharmacology and experimental validation. Methods: Network pharmacology was employed to identify the potential targets and signaling pathways of YSHS in treating DKD, which was hypothesized to be associated with endoplasmic reticulum stress and apoptosis, and these predictions were validated through animal and cellular experiments. Following a 12-week YSHS intervention in db/db mice, assessments were conducted on blood glucose, lipid levels, renal function indices (24-h urinary protein, blood glucose, serum creatinine, blood urea, and urinary albumin-to-creatinine ratio), and kidney pathology. Apoptosis in mouse podocyte clone-5 (MPC-5) cells was assessed using TUNEL labeling. The expression levels of GRP78, PERK, p-PERK, CHOP, Bcl-2, Bax, and Nephrin proteins and mRNAs in mouse kidney tissues and MPC-5 cells were evaluated by immunohistochemistry, Western blotting, and real-time PCR. Results: YSHS significantly improved the general status of db/db mice, with a significant reduction in body mass, renal function indices, total cholesterol, triglycerides, and low-density lipoprotein. Pathological staining showed reduced renal tissue damage in mice, and electron microscopy revealed reduced pedunculopontine fusion and basement membrane thickening. YSHS decreased GRP78, PERK, p-PERK, CHOP, and Bax proteins and mRNA levels in renal tissues and MPC-5 cells ( Conclusion: YSHS inhibited podocyte apoptosis, protected the glomerular filtration barrier, attenuated proteinuria, and improved renal function indices by activating the GRP78/CHOP signaling pathway in the kidneys and the

Indexed as

apoptosisdiabetic kidney diseaseendoplasmic reticulum stresspodocyte damageYi-Shen-Hua-Shi

Identifiers

PMID41020010
PMCPMC12464004

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