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, PGE2 and TNF-α.
 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, PGE2 and TNF-α by using their specific assays. In addition, Histological examination of edema paw was performed to evaluate the anti-inflammatory 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 PGE2 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-α 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, PGE2 and TNF-α at the site of inflammation.
Highlights
The basic essence of pathophysiology of inflammation reveals that our body respond by releasing certain chemicals in response to the noxious agents, infections, and physical injuries to counteract their deleterious effects, if inflammation is uncontrolled it can become a cause of suffering, leading to disabilities, contractures, disfiguring of body, and chronic pain
Carrageenan induced edema was remarkably diminished by prior administration of Commiphora opobalsamum (CO) in the dose of 250 and 500mg/kg body weight. (Fig. 2) when CO in the dose of 250mg/kg was compared with control constantly after 1 hr to 4 hrs p value significance was demonstrated as 1 h p value
It is noteworthy to emphasize that the shrinkage in the development of the swelling in the paw were quite evident in contrast to diclofenac at 1st (p
Summary
The basic essence of pathophysiology of inflammation reveals that our body respond by releasing certain chemicals in response to the noxious agents, infections, and physical injuries to counteract their deleterious effects, if inflammation is uncontrolled it can become a cause of suffering, leading to disabilities, contractures, disfiguring of body, and chronic pain In such situations, the inflammation needs to be controlled or suppressed [1,2]. 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. NO, PGE2 and TNF-α at the site of inflammation
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