Substance P blocks ethanol-induced hepatotoxicity.

Area of Science:

• Hepatology
• Toxicology
• Pharmacology

Background:

• Excessive alcohol consumption causes liver injury and lipid accumulation, contributing to alcoholic liver disease (ALD).
• Protecting hepatocytes from alcohol-induced death is crucial for preventing liver disease progression.
• Substance P (SP) demonstrates cell-protective and proliferative effects under stress, indicating therapeutic potential for liver injury.

Purpose of the Study:

• To investigate the protective effects of Substance P (SP) against ethanol-induced hepatic damage.
• To evaluate the efficacy of SP in both in vitro and in vivo models of alcohol-induced liver injury.

Main Methods:

• SP was administered to ethanol-treated hepatocytes and a mouse model.
• Assessed hepatocyte viability, apoptosis, and Akt/GSK-3β signaling pathway.
• Analyzed liver histology and serum biochemical parameters in mice.

Main Results:

• SP prevented ethanol-induced hepatocyte death in vitro by upregulating Akt/GSK-3β activation.
• In vivo, SP treatment reversed ethanol-induced increases in serum alanine transaminase and apoptotic cells.
• SP administration mitigated lipid accumulation in liver tissue in the mouse model.

Conclusions:

• Substance P effectively blocks hepatic damage caused by ethanol-induced oxidative stress.
• SP exhibits therapeutic effects in liver injury models, including alcoholic liver disease (ALD).
• SP treatment is identified as a promising therapeutic strategy for alcohol-induced hepatic damage.