Abstract
Background: Our recent past studies accomplished the target to investigate the anti-inflammatory effect as well as toxicological profile of Commiphora opobalsamum (CO), with almost identical potency in comparison to the contemporary anti-inflammatory drugs. This inspired us to explore its mechanism of action to further strengthen its efficacy.
Aim: To investigate the mechanism of anti-inflammatory action of CO by exploration of its correlation to its antioxidant activity as well as inhibitory effect on inflammatory mediators by interaction with MDA, NO, PGE(2) and TNF-alpha.
Methods: 10 weeks old male Swiss albino mice (30 to 40 g) were used. Carrageenan-induced paw edema method was used, pretreatment with CO alone in different doses and in combination with diclofenac was done prior to carrageenan administration, subsequently homogenate of the paw was used to quantify the levels of MDA, NO, PGE(2) and TNF-alpha by using their specific assays. In addition, Histological examination of edema paw was performed to evaluate the antiinflammatory effect of CO extract versus diclofenac and control investigating their impact on the inflammatory cell migration and edema formation.
Results: CO extract in the dose of 500mg/kg demonstrated maximum reduction of MDA level; hence antioxidant activity of CO could be contributed to its anti-inflammatory effect. Furthermore, notable observation indicated that CO administration significantly suppress increment in NO level in response to carrageenan, unequivocally significant inhibition of PGE(2) accumulation at the site of inflammation by the pretreatment of CO extract was observed in the dose of 500mg/kg (0.001). Finally in contrast, the CO extract in the dose of 500mg/kg significantly accomplished the reduction of TNF-alpha in the paw in comparison to the control group (p<0.05).
Conclusion: In this study we have illustrated a pioneering perspective to elucidate the mechanism of anti- inflammatory and antioxidant action of methanolic extract of CO, attributed through suppression of MDA. NO, PGE(2) and TNF-alpha at the site of inflammation.