Inflammatory pain and response

A newly discovered role for the use of the SOD mimetic M40403 is as a reliever from inflammatory pain. Wang etal. have proposed that superoxide anions generated in response to inflammatory stimuli are mediators of pain.66 This manganese-containing agent modulates hyperalgesia or excessive sensitiveness to pain via a nociceptive (nerve) signaling cascade (Figure 9.3). Rats were injected with carrageenan (a colloid derived from moss and algae) to produce peripheral inflammation in the paws and other markers of oxidative stress. When a SOD mimetic was administered via intravenous or intrathecal injection, all measures of inflammation and hyperalgesia were inhibited and the

Figure 9.3 Inflammatory stimuli generate superoxide that plays a major role in pain. The MnSOD mimetic, M40403, inhibits the effects of superoxide at both peripheral and central sensitization (based on Ref. 66). Reproduced by permission of the American Society for Pharmacology and Experimental Therapeutics©

Figure 9.3 Inflammatory stimuli generate superoxide that plays a major role in pain. The MnSOD mimetic, M40403, inhibits the effects of superoxide at both peripheral and central sensitization (based on Ref. 66). Reproduced by permission of the American Society for Pharmacology and Experimental Therapeutics©

endogenous SOD2 was deactivated via nitration. Subsequently, the dysfunctional SOD2 was unable to eradicate the superoxide ions, suggesting their involvement in the nociceptive (nervous) pathway. Clearly this new therapeutic approach could lead to a new array of treatments for hyperalgesic response.

Another way to treat inflammation from paw edema resulting from carra-geenan injection is the administration of the chimeric recombinant SOD2/3.36 Whereas an injection of the native SOD2 produced a modest, non-significant response, SOD2/3 decreased edema by 62%. Also, SOD2/3 was compared to the native SOD in a rat model of acute lung injury. When interleukin (IL) 1a was administered by intratracheal instillation, SOD2/3 totally blocked the accumulation of neutrophils and lung leak. Thus this recombinant of SOD appears to be a powerful anti-inflammatory agent for future clinical applications.

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