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Published on: January 10, 2025
Ambroxol alleviates hepatic ischemia reperfusion injury by antioxidant and antiapoptotic pathways
1Department of General Surgery, the Fifth Affiliated Hospital of Harbin Medical University, Daqing, Heilongjiang Province, China.
Background:
Hepatic ischemia/reperfusion (HI/R) injury is a common pathologic process caused by many clinical settings, such as liver resection, liver transplantation, hypovolemic shock, and trauma. The use of ambroxol, which acts as a mucolytic agent, provides antioxidant and anti-inflammatory effects.
Methods:
A rat model of HI/R was induced by clamping the hepatic artery, the hepatoportal vein, and the bile duct with a vascular clamp for 30 minutes followed by reperfusion for 6 hours under anesthesia. The sham group underwent laparotomy without hepatic ischemia. The ambroxol group was injected into the tail vein in the ambroxol group 5 minutes before HI/R at one dose of 20 mg/kg, 80 mg/kg, or 140 mg/kg. The control group underwent the same procedure as the ambroxol group but with administration of physiological saline. Liver injury was evaluated by biochemical and histopathological examinations. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were assayed in serum samples. Superoxide dismutase (SOD), catalase (CAT), malondiadehyde (MDA), and glutathione (GSH) were spectrophotometrically measured. Furthermore, caspase-3, Bcl-2 and Bax expression as well as the level of c-Jun N-terminal kinases (JNK) we estimated activation.
Results:
Wistar rats that received 20, 80 mg or 140 mg of ambroxol displayed reduced HI/R injury compared with controls. Use of ambroxol reduced the histologic injury and significantly decreased serum ALT and AST levels. In addition, ambroxol enhanced the activity of hepatic tissue SOD and CAT, increasing GSH but decreasing MDA tissue contents. In the ambroxol group, Bcl-2 expression was increased and Bax and caspase-3 decreased compared with the controls. Furthermore, ambroxol reduced levels of phosphorylated JNK (P < .05).
Conclusion:
These results indicated that ambroxol attenuated rat HI/R through upregulation of intracellular antioxidant and anti-apoptotic signaling pathways.
Insights
Ambroxol, a mucolytic agent, significantly reduced hepatic ischemia/reperfusion (HI/R) injury in rats. It protected the liver by enhancing antioxidant and anti-apoptotic pathways.
Area of Science:
- Hepatology
- Pharmacology
- Biochemistry
Background:
- Hepatic ischemia/reperfusion (HI/R) injury is a critical clinical issue in liver surgery and transplantation.
- Ambroxol, known for its mucolytic properties, also exhibits potential antioxidant and anti-inflammatory effects.
Purpose of the Study:
- To investigate the protective effects of ambroxol against HI/R injury in a rat model.
- To elucidate the underlying antioxidant and anti-apoptotic mechanisms of ambroxol in HI/R injury.
Main Methods:
- A rat model of HI/R was established, with ambroxol administered intravenously at varying doses (20, 80, 140 mg/kg) prior to reperfusion.
- Liver injury was assessed via biochemical markers (ALT, AST), histopathology, and measurement of oxidative stress markers (SOD, CAT, MDA, GSH).
- Apoptotic markers (caspase-3, Bcl-2, Bax) and JNK signaling pathway activation were also evaluated.
Main Results:
- Ambroxol treatment dose-dependently reduced HI/R-induced liver damage, evidenced by improved histology and lower serum ALT/AST levels.
- Ambroxol significantly increased antioxidant enzyme activity (SOD, CAT) and glutathione levels, while decreasing lipid peroxidation (MDA).
- The drug upregulated anti-apoptotic protein Bcl-2 and downregulated pro-apoptotic proteins Bax and caspase-3, alongside inhibiting JNK phosphorylation.
Conclusions:
- Ambroxol demonstrates significant hepatoprotective effects against HI/R injury in rats.
- These protective effects are mediated by the enhancement of intracellular antioxidant defenses and the suppression of apoptotic signaling pathways.
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