Effect of thymoquinone on transient receptor potential melastatin (TRPM) channels in rats with liver ischemia reperfusion model in rats

Kerem Caglar ¹, Recep Dokuyucu ², Gokhan Agturk ^3,4

⁰Department of Physiology, School of Medicine, Hatay Mustafa Kemal University, Hatay, Turkey.

Iranian Journal of Basic Medical Sciences +

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February 9, 2024

View abstract on PubMed

Summary

Thymoquinone (Tmq) reduces liver damage from ischemia-reperfusion (I/R) injury by decreasing TRPM gene expression and inhibiting calcium entry. This suggests Tmq

Area Of Science

Hepatology
Molecular Biology
Pharmacology

Background

Ischemia-reperfusion (I/R) injury is a significant cause of liver damage.
Transient receptor potential melastatin (TRPM) channels play a role in cellular responses to I/R.
Thymoquinone (Tmq) is a natural compound with potential therapeutic properties.

Purpose Of The Study

To investigate the effect of thymoquinone (Tmq) on hepatic I/R injury in a rat model.
To examine Tmq's impact on TRPM gene expression and its antioxidant and histopathologic effects.

Main Methods

A rat model of hepatic I/R was established.
Rats were divided into control, sham, I/R, Tmq, and Tmq+I/R groups.
Liver tissues and blood were analyzed for histopathology, biochemistry, and TRPM gene expression.

Main Results

Tmq treatment significantly reduced histopathological markers of liver injury, including apoptosis.
Biochemical markers of liver damage (AST, ALT, GGT, LDH) were significantly lower in the Tmq+I/R group compared to the I/R group.
Tmq+I/R treatment led to a significant decrease in TRPM2, 6, 7, and 8 gene expression compared to I/R alone.

Conclusions

Thymoquinone inhibits Ca+2 influx by downregulating TRPM2, 6, 7, and 8 gene expression.
Tmq demonstrates therapeutic potential for liver diseases associated with I/R injury, mitigating both ischemia and apoptosis.
Tmq may be a valuable agent in treating liver-related conditions involving I/R damage.

Keywords:

Cation channels Injury Ischemia-reperfusion TRPM Thymoquinone