Bromelain reduced pro-inflammatory mediators as a common pathway that mediate antinociceptive and anti-anxiety effects in sciatic nerve ligated Wistar rats

Abstract

The involvement of pro-inflammatory mediators complicates the complex mechanism in neuropathic pain (NP). This study investigated the roles of bromelain against pro-inflammatory mediators as a mechanism that underpins its antinociceptive and anti-anxiety effects in the peripheral model of NP. Sixty-four male Wistar rats randomly divided into eight groups, were used for the study. A chronic constriction injury model of peripheral neuropathy was used to induce NP. Tail-immersion and von Frey filaments tests were used to assess hyperalgesia while open field and elevated plus mazes were used to assess anxiety-like behaviour. NF-кB, iNOS, nitrate, and pro-inflammatory cytokines were investigated in the plasma, sciatic nerve, and brain tissues using ELISA, spectrophotometer, and immunohistochemistry techniques after twenty-one days of treatment. Bromelain significantly (p < 0.05) improved the cardinal signs of NP and inhibited anxiety-like behaviours in ligated Wistar rats. It mitigated the increases in cerebral cortex interleukin (IL) -1β, IL-6, and PGE2 levels. Bromelain reduced NF-кB, IL-1β, IL-6, TNF-α, PGE2, and nitrate concentrations as well as the expression of iNOS in the sciatic nerve. Hence, the antinociceptive and anxiolytic effects of bromelain in the sciatic nerve ligation model of NP is in part due to its ability to reduce nitrosative and inflammatory activities.

Chondroitin and glucosamine sulphate reduced proinflammatory molecules in the DRG and improved axonal function of injured sciatic nerve of rats

“…It is interesting to note that suppression of IL1-β might be responsible for the reduction in the level of PGE 2 observed. Our findings showed that IL1-β expression can result to the activation of proinflammatory molecules such as IL-6, SP, PGE 2 through complex signalling cascades [44][45][46] . Evidence has shown that IL1-β just like NGF can modulate excitability of neurons via TRPV1, GABA receptors, sodium channels and NMDA receptors 34 .…”

Chondroitin Sulphate and Glucosamine Sulphate Synergistically Reduced DRG Proinflammatory Molecules and Improved Axonal Function in Sciatic Nerve Ligated Rats.

“…It is interesting to note that suppression of IL1-β might be responsible for the reduction in the level of PGE 2 observed. Our ndings showed that IL1-β expression can result to the activation of proin ammatory molecules such as IL-6, SP, PGE 2 through complex signalling cascades [53,54,55]. Evidence has shown that IL1-β just like NGF can modulate excitability of neurons via TRPV1, GABA receptors, sodium channels and NMDA receptors [43].…”

The Causal Role of Magnesium Deficiency in the Neuroinflammation, Pain Hypersensitivity and Memory/Emotional Deficits in Ovariectomized and Aged Female Mice

“… 69 Accumulative experimental evidence has demonstrated that the overproduction of these inflammatory cytokines is necessary and even sufficient to induce chronic pain, memory decline and mood depression in rodents. 7 , 8 , 70 , 71 It has been proposed that the estrogen decline-induced neuronal disorders are mediated by inflammation. 14 While how estrogen decline causes inflammation in nervous system remains unclear.…”