Healing and preventive effects of low-esterified pectin on liver injury inducedby carbon tetrachloride in rats > Volume 04 - 2004

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Oriental Pharmacy and Experimental Medicine
Volume 04 - 2004
Date: 2004

Journal: Pages 28-36

March 2004 | Healing and preventive effects of low-esterified pectin on liver injury inducedby carbon tetrachloride in rats…

Yuri S Khotimchenko1,2,*,Elena A Kolenchenko1,Maxim Y Khotimchenko2andValeri V Kovalev1



​The purpose of this study was to investigate the pharmacological effects of low-esterified pectinon carbon tetrachloride (CCL4)-induced hepatotoxicity in rats. The study included two experiments.In the first experiment the animals were given daily CCL4 through gavage for 7 days and then 10,50, or 250mg/kg b.w. of pectin for 21 days. At the end of experiment rats were killed within 24 hours. Theincreased bilirubin level, enhanced alanine aminotransferase and aspartate aminotransferase activity inplasma induced by CCL4 were partly normalized by pectin administration in a dose-dependentmanner. The pectin treatment also resulted in significant recovery of CCl4-induced decrease of theliver glycogen content. In addition, pectin significantly improved CCL4-induced alterations ofpro-oxidant and antioxidant biochemical parameters in liver and plasma compared to those ofrats administered CCL4. In the second experiment the animals were given daily 10, 50 or 250 mg/kg b.w. of pectin for 21 days before a 7-day administration of CCL4. Rats were killed 24 hoursafter the end of experiment. Pretreatment with pectin before CCL4 administration resulted insignificantly inhibited increase of the blood enzymatic activities of alanine and aspartateaminotransferases and bilirubin level in a dose-dependent manner. Also, preliminary administration ofpectin prevented elevation of malondialdehyde and conjugated diene levels in liver and plasmaas well as a reduction of glutathione content in liver of rats given CCL4. These results suggest thatlow-esterified pectin exert healing and preventive effects on CCL4-induced hepatotoxicity in rats.

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