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Published on: February 15, 2022
Renal Tissue Damage Induced by Acute Kidney Injury in Sepsis Rat Model Is Inhibited by Cynaropicrin via IL-1β and
Danlei Cai1, Hongdan Duan2, Yangshan Fu2
1Department of Emergency Medicine, Affiliated Hospital of Nantong University, Nantong, Jiangsu, China.
Abstract:
Acute kidney injury (AKI), one of the frequently diagnosed and serious sepsis induced complication has high morbidity and mortality. The present study investigated the effect of cynaropicrin on AKI induced pathological damage in rat model in vivo. Treatment with cynaropicrin suppressed AKI induced urea nitrogen and creatinine in the rat serum in dose-dependent manner. Development of sepsis mediated renal injury in rats was also effectively prevented on treatment with cynaropicrin. Secretion of AKI-induced IL-1β and TNF-α in renal tissues was alleviated significantly in rats by cynaropicrin treatment. Additionally, in cynaropicrin-treated rats renal tissues AKI induced Bax expression was alleviated while as Bcl-2 was promoted compared to AKI rats. Cynaropicrin treatment improved the survival rate of the rats with AKI. Cynaropicrin inhibits renal tissue damage and increase survival rate in AKI rat model. The mechanism involves alleviation of inflammatory cytokine secretion and promotion of Bcl‑2 expression. Thus, cynaropicrin may be used as therapeutic agent for treatment of AKI.
Insights
Cynaropicrin effectively treats acute kidney injury (AKI) in rats by reducing kidney damage and improving survival rates. This sepsis-induced complication is mitigated through reduced inflammation and apoptosis.
Area of Science:
- Nephrology
- Pharmacology
- Immunology
Background:
- Sepsis-induced acute kidney injury (AKI) is a severe complication with high morbidity and mortality.
- Current therapeutic options for AKI are limited, necessitating the exploration of novel treatments.
Purpose of the Study:
- To investigate the protective effects of cynaropicrin against sepsis-induced AKI in a rat model.
- To elucidate the underlying mechanisms of cynaropicrin's renoprotective action.
Main Methods:
- Rats were subjected to sepsis to induce AKI.
- Cynaropicrin was administered at varying doses to assess its therapeutic potential.
- Serum markers (urea nitrogen, creatinine), inflammatory cytokines (IL-1β, TNF-α), and apoptosis-related proteins (Bax, Bcl-2) were analyzed.
- Survival rates were monitored.
Main Results:
- Cynaropicrin treatment significantly reduced serum urea nitrogen and creatinine levels in a dose-dependent manner.
- Renal injury and inflammation, indicated by decreased IL-1β and TNF-α secretion, were ameliorated by cynaropicrin.
- Cynaropicrin modulated apoptosis by decreasing Bax expression and increasing Bcl-2 expression.
- Survival rates in rats with AKI were significantly improved following cynaropicrin treatment.
Conclusions:
- Cynaropicrin demonstrates significant renoprotective effects in a sepsis-induced AKI rat model.
- The therapeutic mechanism involves the suppression of inflammatory cytokine secretion and the modulation of apoptosis.
- Cynaropicrin holds potential as a therapeutic agent for treating acute kidney injury.
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Acute Kidney Injury II: Pathophysiology
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