Morinda lucida stem bark reversed the pattern and extent of lead nitrate-induced liver injury in Wistar rats.

Lead toxicity remains one of the most important occupational and environmental health problems with characteristic features that are incompatible with life. Considering the foregoing, we investigated the ameliorative potentials of Morinda lucida stem bark (MLSB) extract on lead nitrate-induced hepatic injury with particular emphasis on its effects on the pattern and extent of lead nitrate toxicity. Thirty-six adult Wistar rats were randomly assigned into six groups (n=6). Normal control group received 2.2mL/kg distilled water only for 4 weeks while hepatic injury was induced by 2-week oral administration of 30mg/kg lead nitrate to experimental rats in the remaining five groups. Following induction, test groups were treated with MLSB for another 2 weeks at 100, 250, and 500mg/kg concentrations respectively while silymarin was administered orally for 2 weeks to positive control group. At the end of the study, serum activities of liver function enzymes and tissue levels of malondialdehyde were determined. Patterns and extent of injury were determined in hematoxylin and eosin-stained section. The result revealed a significant reduction in sera levels of liver function enzymes and tissue level of malondialdehyde (MDA) in extract treated groups. Lead nitrate-induced necrotic changes and other deranged features observed in histological sections were multifocal and they span through multiple zones of hepatic acini (panacinar), MLSB at 250mg/kg concentration reversed by some of these effects. The study concluded that ameliorative property of MLSB could be due to the antioxidant and membrane stabilizing properties of its phenolic compounds.

Ethanol extract of Curcuma longa rhizome mitigates potassium bromate-induced liver changes in the Wistar rat: Histological, histochemical and immunohistochemical assessments.

The effects of Curcuma longa rhizome on hepatic cells, glycogen, connective tissue fibres and filamentous cytoskeleton were evaluated following KBrO3-induced liver injury in Wistar rats. Thirty-five male rats were randomly divided into seven groups (n=5). Group 1 were normal saline treated rats. Hepatic injury was induced in groups 2 to 7 by oral administration of 100mg/kg KBrO3 for 2 weeks. Following induction, rats in group 2 were sacrificed while groups 3, 4, 5 were given oral dose of EECLOR at 100, 200, 400mg/kg respectively. Group 6 rats were treated with silymarine while group 7 rats were left untreated. The rats were sacrificed and the liver sections were stained with H&E, Masson trichrome, Gordon and Sweets, PAS, Feulgen reaction, anti-vimentin antibody for demonstration of general histoarchitecture, elastic fibre, collagen fibre; glycogen, nuclear DNA and filamentous cytoskeleton respectively. Groups 2, 3, 7 developed intranuclear vacuolation, plasma coagulation, plamolysis, karyopyknosis, karyorrhexis and karyolysis, hyperchromatism, DNA fading and pleomorphism. Immunohistochemical study revealed near negative immunoreaction for vimentin. These pathological changes were ameliorated in EECLOR-treated groups in a manner comparable to silymarine-treated group. The study concluded that ameliorative effects of EECLOR in KBrO3-induced liver injury could be due to its vimentin stabilization property.