The Effect of Moringa Isothiocyanate-1 on Renal Damage in Diabetic Nephropathy

Authors

  • Lijing Chen Department of Nephrology, Huzhou Central Hospital and Affiliated Central Hospital Huzhou University, 313000 Huzhou, Zhejiang, China
  • Deyong Fan Department of Nephrology, Huzhou Central Hospital and Affiliated Central Hospital Huzhou University, 313000 Huzhou, Zhejiang, China
  • Fei Guo Department of TCM Acupuncture, Huzhou Central Hospital and Affiliated Central Hospital Huzhou University, 313000 Huzhou, Zhejiang, China
  • Jiuhong Deng Wenzhou Medical University. Wenzhou Medical University, Chashan Higher Education Park, Wenzhou, Zhejiang, China; The Second Affiliated Hospital Zhejiang University, School of Medicine, 310009 Hangzhou, Zhejiang, China
  • Linlin Fu Department of Pathology, Huzhou Central Hospital and Affiliated Central Hospital Huzhou University, 313000 Huzhou, Zhejiang, China

Abstract

Introduction. Diabetic nephropathy (DN) is the most common clinical complication of diabetes mellitus. Moringa isothiocyanate-1 (MIC-1) is effective in the treatment of diabetes mellitus, but its mechanism of action in DN remains obscure. This research specifically probed the role of MIC-1 in modulating renal injury in DN. Methods. Six db/m mice were assigned to control group and twelve db/db mice were randomly allocated to the db/db and db/db + MIC-1 groups. The body and kidney weights of the mice were monitored. Renal function indicators and oxidative stress-related markers were assessed by automatic biochemical analyzer and ELISA method. The pathological changes, apoptosis of renal tissues, extracellular regulated protein kinases (ERK) 1/2/ Nuclear factor erythroid2-related factor 2 (Nrf2) pathway-related markers, and the positive expressions of podocalyxin (Pod) and synaptopodin (Syn) were measured by H&E, PAS, and TUNEL staining, Western blot, and IHC assay. Results. MIC-1 reduced the body and kidney weights, and increased the kidney organ index (calculated as 100*kidney weight/ body weight) in db/db mice. In addition, MIC-1 improved renal function, kidney tissue injury, and apoptosis of db/db mice. MIC1 noticeably repressed the contents of reactive oxygen species (ROS) and malondialdehyde (MDA) and enhanced the contents of (glutathione) GSH, superoxide dismutase (SOD), and catalase (CAT) in db/db mice. At molecular level, db/db mice showed a decrease in p-ERK/ERK, Nrf2, SOD-1, heme oxygenase 1 (HO-1), and CAT and an increase in p- inhibitor kappa B alpha (IKBα) and p-Nuclear factor-kappa B (P65/P65), which were reversed when MIC-1 was administered. Furthermore, MIC-1 facilitated the positive expressions of Pod and Syn of the kidney tissues in db/db mice. Conclusion. MIC-1 reduces oxidative stress and renal injury by activating the ERK/Nrf2/HO-1 signaling and repressing the NFκB signaling in db/db mice.

 

DOI: 10.52547/ijkd.7515

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Published

2023-10-12

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Section

ORIGINAL | Kidney Diseases