Abstract
The expression of mitochondrial voltage-dependent anion channels (VDAC) mayunderlie the protective effects of Limonium sinense (Girard) Ktze root extracts (LSE) againstcarbon tetrachloride-induced liver damage. Pretreatment of mice with 100 mg/kg, 200mg/kg or 400 mg/kg LSE significantly blocked the carbon tetrachloride-induced increase inboth serum aspartate aminotransferase (sAST) and serum alanine aminotransferase (sALT)levels. Ultrastructural observations by electron microscope confirmed hepatoprotection,showing decreased nuclear condensation, ameliorated mitochondrial fragmentation of thecristae and less lipid deposition. Pretreatment with LSE prevented the decrease of thedisruption of mitochondrial membrane potential (15.3%) observed in the liver of the carbontetrachloride-insulted mice, further demonstrating the mitochondrial protection. In addition,LSE treatment (100-400 mg/kg) significantly increased both transcription and translation ofVDAC. The above data suggests that LSE mitigates the damage to liver mitochondriainduced by carbon tetrachloride, possibly through regulation of mitochondrial VDAC, one ofthe most important proteins in the mitochondrial outer membrane.
Highlights
Evidence has accumulated that cell death is involved in liver injury and liver disease
We evaluated the hepatoprotective effect of Limonium sinense (Girard) Ktze (LSE) extracts against liver injury induced by CCl4, addressing the possible action of LSE on liver mitochondrial and voltage-dependent anion channel (VDAC) expression to search for the mechanism underlying its hepatoprotective activity
The results of the present study show that 100 mg/kg, 200 mg/kg or 400 mg/kg LSE significantly protect mice against CCl4-induced hepatotoxicity, as demonstrated by its inhibition of the elevation of serum aspartate aminotransferase (sAST) and serum alanine aminotransferase (sALT)
Summary
Evidence has accumulated that cell death is involved in liver injury and liver disease. Apoptosis and necrosis underlie many types of liver injury, including fibrosis, alcoholic liver disease and hepatitis [1, 2]. Mitochondrial dysfunction contributes to a great number of human and animal diseases. Changes such as disruption in mitochondrial membrane potential occur in the process of liver injury and drugs could protect liver mitochondrial through preventing the dissipation of mitochondrial membrane potential in hepatotoxicated mice [4, 5, 6]. We evaluated the hepatoprotective effect of Limonium sinense (Girard) Ktze (LSE) extracts against liver injury induced by CCl4, addressing the possible action of LSE on liver mitochondrial and VDAC expression to search for the mechanism underlying its hepatoprotective activity
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