1. Academic Validation
  2. Carnosine Protects Mouse Podocytes from High Glucose Induced Apoptosis through PI3K/AKT and Nrf2 Pathways

Carnosine Protects Mouse Podocytes from High Glucose Induced Apoptosis through PI3K/AKT and Nrf2 Pathways

  • Biomed Res Int. 2019 May 28;2019:4348973. doi: 10.1155/2019/4348973.
Kunxiao Zhao 1 Ying Li 1 Ziqiang Wang 2 Ning Han 1 Ying Wang 3
Affiliations

Affiliations

  • 1 Department of Nephrology, The Third Hospital of Hebei Medical University, Shijiazhuang, Hebei Province 050051, China.
  • 2 Department of Nephrology, Cangzhou People's Hospital, Cangzhou, Hebei Province 061000, China.
  • 3 Department of Nephrology, BayanNur Hospital, Bayan Nur, Inner Mongolia Autonomous Region 015000, China.
Abstract

Diabetic nephropathy is the complication of diabetes mellitus that can lead to chronic renal failure. Reactive Oxygen Species (ROS) production plays an important role in its pathological process. Previous studies showed that carnosine may reduce diabetic nephropathy by antioxidant effect. However, the molecular mechanism of its antioxidant was not fully understood. In the current study, we developed high glucose containing different concentrations of carnosine to reduce ROS levels and podocytes Apoptosis, and Cell Counting Kit-8 test was used to observe the cell viability. Carnosine (5-20mM) was found to protect mouse podocytes (MPC5) cells from HG-induced injury. Quantitative Real-Time PCR, Western blotting, and immunofluorescence staining revealed that high glucose induced ROS levels and podocytes Apoptosis were downregulated by PI3K/Akt and Nrf2 signaling pathways. The current findings suggest that carnosine may reduce ROS levels and MPC5 cells Apoptosis by PI3K/Akt and Nrf2 signaling pathways activation.

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