ArticleAging2024
Ginsenoside Rg3 induces mesangial cells proliferation and attenuates apoptosis by miR-216a-5p/MAPK pathway in diabetic kidney disease.
Article in Aging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Effectiveness and safety of Tongxinluo capsule for diabetic kidney disease: A systematic review and meta-analysis.World journal of diabetes · 2025Article
- Mesangial Cells in Diabetic Kidney Disease: From Mechanisms to Therapeutic Implications.International journal of biological sciences · 2025Review
- Ginsenoside in the treatment of type 2 diabetes and its complications: a promising traditional chinese medicine.Frontiers in pharmacology · 2025Review
- MiR-216a-5p protects against high glucose-induced HMC injury by targeting the HMGB1/RAGE signaling pathway.Frontiers in endocrinology · 2025Article
- Advances in ginsenoside treatment for common kidney diseases: pharmacological evaluation and potential mechanisms.Frontiers in pharmacology · 2025Review
- Renal Health Through Medicine-Food Homology: A Comprehensive Review of Botanical Micronutrients and Their Mechanisms.Nutrients · 2024Review
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Authors and funding
5 authors.
Funding
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Abstract
backgroundGinsenoside Rg3 is an active saponin isolated from ginseng, which can reduce renal inflammation. However, the role and mechanism of Rg3 in diabetic kidney disease (DKD) are far from being studied.
methodsThe effects of Rg3 and miR-216a-5p on the proliferation, apoptosis, and MAPK pathway in high glucose (HG)-induced SV40 MES 13 were monitored by CCK-8, TUNEL staining, and western blot.
resultsRg3 treatment could accelerate proliferation and suppress apoptosis in HG-induced SV40 MES. Moreover, miR-216a-5p inhibition also could alleviate renal injury, prevent apoptosis, and activate the MAPK pathway in kidney tissues of diabetic model mice.
conclusionRg3 could attenuate DKD progression by downregulating miR-216a-5p, suggesting Rg3 and miR-216a-5p might be the potential drug and molecular targets for DKD therapy.
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