Protein dependent fate of hepatic cells under nicotine induced stress and curcumin ameliorated condition

摘要: Nicotine is mainly metabolized in liver. Its abuse elicits acute phase response by activating macrophages to produce pro-inflammatory cytokines, which play critical role apoptosis or cell proliferation. The protective pharmacological mechanism of curcumin against nicotine-induced toxicity on protein malnourished liver still remaining unclear. This study investigated the ameliorative and also fate particularly under restricted condition. Female Albino-rats maintained normal/protein-restricted diets, were subcutaneously injected with nicotine tartrate (2.5 mg/kg body weight/day) orally supplemented (80 for 21 days. animals then sacrificed dissect out proceed further experiments. Interactions DNA both vivo vitro observed thermal denaturation laddering assays. Effects hepatic cells monitored differential staining, comet assay, cytokine profiling, mRNA expression. caused more intense damage, promoted death through up-regulating pro-apoptotic proteins signaling molecules individuals. Through up-regulation anti-apoptotic proliferation promoting molecules, dysregulated homeostasis normal Curcumin significantly ameliorated conditions regulated imbalance between survival induced nicotine. content present decides either cell-survival pathway cytotoxic pathway.