Cynomorium songaricum Rupr. Polysaccharide (CSP) Attenuates Diabetic Nephropathy by Activating AMPK/SIRT1 Signalling
- Clin Exp Pharmacol Physiol. 2026 Jun;53(6):e70138. doi: 10.1111/1440-1681.70138.
- 1. Department of Nephrology and Rheumatology, The ChenJiaqiao Hospital of ShaPingba District of Chongqing City, Chongqing, People's Republic of China.
- 2. Department of Emergency, the Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei province, People's Republic of China.
- 3. Key Laboratory for Molecular Diagnosis of Hubei Province, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, People's Republic of China.
- 4. Department of Intensive Care Union, The ChenJiaqiao Hospital of ShaPingba District of Chongqing City, Chongqing, People's Republic of China.
Objective: Diabetic nephropathy (DN) represents a significant complication of diabetes and serves as a primary trigger for end-stage renal disease. The study aimed to investigate the renal protective influence of Cynomorium songaricum Rupr. polysaccharide (CSP) on inflammation and oxidative stress in DN and explore its related mechanisms.
Methods: High glucose (HG)-stimulated podocytes (MPC-5 cells) were used as the cell model for DN. Cell counting kit-8 assay, flow cytometry analysis, and detection of Lactate Dehydrogenase production were performed to measure cell viability, Apoptosis and cell death. A diabetic mouse model was established through streptozotocin induction. Levels of blood urea nitrogen (BUN), serum creatinine and 24-h urine protein were measured to assess renal function. Immunofluorescence staining of kidney samples was conducted to measure the expression of tumour necrosis factor (TNF)-α and interleukin (IL)-6. Oxidative stress markers of catalase (CAT), superoxide dismutase (SOD) and malondialdehyde (MDA) were measured by corresponding kits. ELISA was performed to assess inflammatory cytokine levels in renal tissue. Western blot was performed to quantify protein levels of factors related to Apoptosis, inflammation, oxidative stress and AMPK/SIRT1 pathway.
Results: CSP protected MPC-5 cells from HG-induced injury by inhibiting cell Apoptosis and death while increasing cell viability. In addition, CSP notably repressed oxidative stress as manifested by an increase in CAT and SOD activities and a decline in MDA content, NOX2 level and NOX4 level. Meanwhile, the significant downregulation of IL-6, TNF-α, IL-1β, COX-2 and iNOS levels was found in HG-treated MPC-5 cells in the context of CSP administration. More importantly, CSP treatment attenuated inflammation and oxidative stress in the renal tissue of DN mice. CSP activated the AMPK/SIRT1 signalling in the renal tissue of DN mice.
Conclusion: CSP inhibits DN progression by alleviating inflammatory response and oxidative stress via activation of the AMPK/SIRT1 signalling.