Related Experiment Video
Updated: Jun 28, 2025
Author Spotlight: Network Pharmacology and Molecular Docking to Decipher the Action of Jiawei Shengjiang San Against Diabetic Kidney Disease
Published on: May 10, 2024
Jiawei Shengjiangsan's Effect on Renal Injury in Diabetic Nephropathy Mice is Investigated via the PI3K/Akt/NF-κB
Chenhua Yang1, Fengling Huang2, Huiqin Fang3
1General Medicine, Bao'an Authentic TCM Therapy Hospital, Shenzhen, Guangdong, People's Republic of China.
Purpose:
This study aimed to investigate the intervention mechanism of Jiawei Shengjiangsan (JWSJS) on kidney injury in diabetic nephropathy mice.
Methods:
Thirty 8-week-old db/db mice were randomly divided into five groups: model group, Perindopril group, and JWSJS low-, medium-, and high-dose groups (n=6 per group) based on body weight. Additionally, a blank control group was established consisting of 6 db/m mice aged 8 weeks. The blank and model groups received daily intragastric administration of 7g/kg/d pure water. The remaining groups were assigned to JWSJS low (3.5g/kg/d), medium (7g/kg/d), high (14g/kg/d) dosage groups, and perindopril positive control group (0.48mg/kg/d) for 12 weeks. Post-experiment, serum creatinine (SCr) and blood urea nitrogen (BUN) were analyzed using an automatic biochemical analyzer. Enzyme-linked immunosorbent assay (ELISA) measured 24-hour urinary albumin, neutrophil gelatinase-associated lipocalin (NGAL), TNF-α, IL-1β, VCAM-1, MCP-1, and HbA1c. Western blot assessed the protein expressions of p-PI3K, p-Akt, and p-NF-κB p65, while pathological kidney changes were observed.
Results:
Compared to the blank group, the model group exhibited increased SCr, BUN, 24-hour urinary albumin, serum NGAL, TNF-α, IL-1β, VCAM-1, MCP-1, HbA1c, p-PI3K, and p-Akt, alongside increased p-NF-κB p65 expression, indicating significant kidney pathology. After treatment, the JWSJS group showed decreased SCr, BUN, 24-hour urinary microalbumin, NGAL, HbA1c, TNF-α, IL-1β, VCAM-1, MCP-1 levels, increased p-PI3K and p-Akt expression (P<0.05), and reduced p-NF-κB p65 content (P<0.05). Histopathological analysis revealed that JWSJS ameliorated renal tubular epithelial cell damage, glomerular capillary and basement membrane injuries, and facilitated the repair of damaged podocytes in diabetic nephropathy mice.
Conclusion:
JWSJS demonstrated efficacy in reducing renal inflammation in diabetic nephropathy mice, with its mechanism likely associated with the inhibition of the PI3K/Akt/NF-κB signaling pathway.
Insights
Jiawei Shengjiangsan (JWSJS) effectively reduced kidney inflammation and injury in diabetic nephropathy mice. Its mechanism involves inhibiting the PI3K/Akt/NF-κB signaling pathway, improving kidney function and pathology.
Area of Science:
- Pharmacology
- Nephrology
- Traditional Chinese Medicine
Background:
- Diabetic nephropathy (DN) is a major complication of diabetes, leading to significant kidney damage.
- Current treatments for DN have limitations, necessitating the exploration of novel therapeutic agents.
- Jiawei Shengjiangsan (JWSJS) is a traditional Chinese medicine with potential renoprotective properties.
Purpose of the Study:
- To investigate the therapeutic mechanism of JWSJS in a mouse model of diabetic nephropathy.
- To evaluate the effects of JWSJS on kidney injury markers and inflammatory pathways.
Main Methods:
- db/db mice were treated with varying doses of JWSJS or Perindopril for 12 weeks.
- Serum creatinine (SCr), blood urea nitrogen (BUN), and urinary albumin were measured.
- Levels of inflammatory cytokines (TNF-α, IL-1β, VCAM-1, MCP-1), NGAL, and HbA1c were assessed via ELISA.
- Protein expression of PI3K/Akt/NF-κB signaling pathway components was analyzed using Western blot.
- Renal histopathology was examined to evaluate kidney damage.
Main Results:
- JWSJS treatment significantly reduced SCr, BUN, urinary albumin, NGAL, HbA1c, and inflammatory markers (TNF-α, IL-1β, VCAM-1, MCP-1) compared to the model group.
- JWSJS upregulated the expression of p-PI3K and p-Akt while downregulating p-NF-κB p65.
- Histological analysis showed JWSJS ameliorated renal tubular and glomerular damage, and improved podocyte injury.
Conclusions:
- JWSJS exhibits significant renoprotective effects in diabetic nephropathy.
- The therapeutic mechanism of JWSJS is associated with the inhibition of the PI3K/Akt/NF-κB signaling pathway.
- JWSJS demonstrates potential as a treatment for diabetic nephropathy by reducing inflammation and improving kidney structure.
More Related Videos
07:15Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
Published on: August 23, 2024
10:37Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice
Published on: May 2, 2025
