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Hepatoprotection through regulation of voltage dependent anion channel expression by Amomum subulatum Roxb seeds
Mihir Y Parmar1, Purvi A Shah, Jing Gao
1Anand Pharmacy College, Opp. Town Hall, Anand, Gujarat, India.
Background And Purpose:
Voltage dependent anion channel (VDAC) plays an important role in triggering the opening of the mitochondrial permeability transition pore (PTP) that leads to mitochondrial damage and induce apoptic or necrotic cell death. In the present study, the methanolic extract of Amomum subulatum Roxb. seeds (MEAS) was used to examine its effect on VDAC. Aminotransferase activity, mitochondrial membrane potential, calcium-induced liver MPT, and VDAC expression were used to evaluate the hepato protective effect of MEAS.
Results:
Pretreatment of mice with MEAS (100 and 300 mg/kg) significantly blocked the CCl(4)-induced increase in AST and ALT activities. Pretreatment with MEAS showed significant preservation of mitochondrial membrane potential as compared to CCl(4) control demonstrating the mitochondrial protection. In addition, pretreatment with MEAS at various concentrations exerted a dose-dependent effect against sensitivity to mitochondrial swelling induced by calcium. In addition, MEAS (300 mg/kg) significantly increased the transcription and translation of VDAC.
Conclusion:
Our data suggest that MEAS significantly prevents the damage to liver mitochondria through regulation of VDAC expression.
Insights
Amomum subulatum Roxb. seeds extract (MEAS) protects liver mitochondria by regulating Voltage Dependent Anion Channel (VDAC) expression. This extract prevents mitochondrial damage and cell death, offering a potential therapeutic approach.
Area of Science:
- Mitochondrial Biology
- Pharmacology
- Hepatoprotective Agents
Background:
- Voltage Dependent Anion Channel (VDAC) is crucial in initiating the mitochondrial permeability transition pore (PTP) opening.
- PTP opening leads to mitochondrial damage, apoptosis, or necrosis.
- Amomum subulatum Roxb. seeds extract (MEAS) was investigated for its effects on VDAC and liver protection.
Purpose of the Study:
- To evaluate the hepatoprotective effects of MEAS.
- To investigate the impact of MEAS on VDAC expression and function.
- To assess MEAS's role in preventing mitochondrial damage.
Main Methods:
- Mice were pretreated with MEAS (100 and 300 mg/kg) before CCl(4) induction.
- Assessed aminotransferase (AST and ALT) activities.
- Evaluated mitochondrial membrane potential, calcium-induced mitochondrial permeability transition (MPT), and VDAC expression.
Main Results:
- MEAS significantly reduced CCl(4)-induced AST and ALT elevation.
- MEAS preserved mitochondrial membrane potential and reduced sensitivity to calcium-induced swelling.
- MEAS (300 mg/kg) increased VDAC transcription and translation.
Conclusions:
- MEAS demonstrates significant hepatoprotective effects.
- MEAS prevents liver mitochondrial damage by regulating VDAC expression.
- This suggests MEAS as a potential therapeutic agent for liver protection.