Evaluation of phytochemicals, antioxidant activity and amelioration of pulmonary fibrosis with Phyllanthus emblica leaves

BACKGROUND In the present study the antioxidant potential of a methanol extract of Phyllanthus emblica leaves (PELE) was determined by in vitro methods as well as by an in vivo animal model, along with HPLC-DAD screening for phyto-constituents. METHODS The in vitro antioxidant potential of PELE was assessed by scavenging of DPPH, nitric oxide and anti-lipid peroxidation assays. For in vivo evaluation, a 60-day experimental plan was followed in which Sprague Dawley rats were administered with 1 mL/kg of CCl4 (CCl4 : DMSO + Olive oil; 30 % v/v) alone or with different doses of PELE (200, 400 mg/kg p.o.). Silymarin (100 mg/kg) as standard drug was also administered to CCl4 treated rats. HPLC-DAD analysis was performed to quantify polyphenolic phytochemicals. RESULTS PELE exhibited an appreciable in vitro antioxidant activity and scavenged the DPPH radical (IC50 = 39.73 ± 2.12 μg/mL) and nitric oxide (IC50 = 39.14 ± 2.31 μg/mL) while for anti-lipid peroxidation moderate antioxidant activity was noticed. Reduced levels of antioxidant enzyme activities viz., superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and reduced glutathione (GSH) whereas enhanced levels of total extractable proteins, lipid peroxides (TBARS), nitrite and H2O2 were induced by CCl4 administration in lungs of rat. Co-administration of PELE to rats exhibited a dose dependent decline in the oxidative injuries induced in these parameters. Histopathological damages such as disrupted alveoli, infiltration of macrophages and modified architecture of Clara cells was reversed to the normal state with co-administration of PELE. HPLC-DAD analysis indicated the presence of gallic acid, rutin, kaempferol and caffeic acid in the PELE. CONCLUSION The findings of this study demonstrate that presence of polyphenolics and other active constituents in PELE might play a significant role in repairing the pulmonary damages instigated with CCl4.