» Articles » PMID: 38149724

Cordyceps Cicadae Polysaccharides Attenuate Diabetic Nephropathy Via the MiR-30a-3p/TRIM16 Axis

Overview
Specialty Endocrinology
Date 2023 Dec 27
PMID 38149724
Authors
Affiliations
Soon will be listed here.
Abstract

Objective: The molecular mechanism of the protective effect of Cordyceps cicadae polysaccharides (CCPs) on renal tubulointerstitial fibrosis in diabetic nephropathy (DN) is still unclear. This study aims to further understand the molecular mechanisms behind the therapeutic benefits of CCP on diabetic nephropathy.

Methods: Mice were randomly assigned into six groups (n = 8). Cordyceps cicadae polysaccharide dissolved in 5% dimethyl sulfoxide was administered by gavage for 12 consecutive weeks. The CCP doses were divided into low, medium, and high, 75, 150, and 300 mg/kg/day, respectively. The efficacy of CCP was determined by assessing the renal function and histological alterations in diabetic db/db mice. The degree of glomerular mesangial dilatation and sclerosis was evaluated using semiquantitative markers. Cell viability, apoptosis, epithelial-mesenchymal transition (EMT), inflammation, oxidative stress, and mitochondrial reactive oxygen species (ROS) in high glucose (HG)-cultured MPC5 podocytes were determined. The interaction of miR-30a-3p and tripartite motif-containing protein 16 (TRIM16) was examined by luciferase reporter assay. Western blotting, reverse transcription-polymerase chain reaction, and immunofluorescence were used to analyze gene and protein expressions.

Results: The in vivo findings illustrated that CCP may protect mice with type 2 diabetes from inflammation and oxidative damage (P < 0.05). Furthermore, CCP has a therapeutic value in protecting renal function and morphology in diabetic nephropathy by reversing podocyte EMT. The in vitro results indicated that CCP dose-dependently inhibited HG-induced apoptosis, EMT, inflammation, oxidative stress, and mitochondrial ROS levels in MPC5 podocytes (P < 0.05). Luciferase reporter assay confirmed the interaction between miR-30a-3p and TRIM16 in MPC5 podocytes cultured in high glucose (P < 0.05).

Conclusion: The protective effect of CCP on HG-induced MPC5 can be achieved by miR-30a-3p/TRIM16 axis.

Citing Articles

Targeting programmed cell death in diabetic kidney disease: from molecular mechanisms to pharmacotherapy.

Liu F, Yang Z, Li J, Wu T, Li X, Zhao L Mol Med. 2024; 30(1):265.

PMID: 39707216 PMC: 11660506. DOI: 10.1186/s10020-024-01020-5.


β-Sitosterol Mitigates Apoptosis, Oxidative Stress and Inflammatory Response by Inactivating TLR4/NF-кB Pathway in Cell Models of Diabetic Nephropathy.

Yang S, Zhang Y, Zheng C Cell Biochem Biophys. 2024; 83(1):1249-1262.

PMID: 39424766 DOI: 10.1007/s12013-024-01559-4.


Noncoding RNAs and diabetic kidney disease.

Wada J J Diabetes Investig. 2024; 16(1):8-9.

PMID: 39361944 PMC: 11693531. DOI: 10.1111/jdi.14331.

References
1.
Joglekar M, Patil D, Joglekar V, Rao G, Reddy D, Mitnala S . The miR-30 family microRNAs confer epithelial phenotype to human pancreatic cells. Islets. 2010; 1(2):137-47. DOI: 10.4161/isl.1.2.9578. View

2.
Wang E, Wang L, Ding R, Zhai M, Ge R, Zhou P . Astragaloside IV acts through multi-scale mechanisms to effectively reduce diabetic nephropathy. Pharmacol Res. 2020; 157:104831. DOI: 10.1016/j.phrs.2020.104831. View

3.
Tang J, Yao D, Yan H, Chen X, Wang L, Zhan H . The Role of MicroRNAs in the Pathogenesis of Diabetic Nephropathy. Int J Endocrinol. 2019; 2019:8719060. PMC: 6914872. DOI: 10.1155/2019/8719060. View

4.
Strasser A, Cory S, Adams J . Deciphering the rules of programmed cell death to improve therapy of cancer and other diseases. EMBO J. 2011; 30(18):3667-83. PMC: 3173800. DOI: 10.1038/emboj.2011.307. View

5.
Mihailovic M, Dinic S, Arambasic Jovanovic J, Uskokovic A, Grdovic N, Vidakovic M . The Influence of Plant Extracts and Phytoconstituents on Antioxidant Enzymes Activity and Gene Expression in the Prevention and Treatment of Impaired Glucose Homeostasis and Diabetes Complications. Antioxidants (Basel). 2021; 10(3). PMC: 8003070. DOI: 10.3390/antiox10030480. View