Ameliorative potential of montelukast on ischemia–reperfusion injury induced vasculitic neuropathic pain in rat

Resveratrol alleviates nuclear factor‐κB‐mediated neuroinflammation in vasculitic peripheral neuropathy induced by ischaemia–reperfusion via suppressing endoplasmic reticulum stress

“…Firstly, this study addressed the protective effects and underlying mechanisms of resveratrol in the early phase of VPN induced by IR. Because this model has been known to produce prolonged behavioural changes in previous studies, the question of whether resveratrol exerts any protective effect in the late phase of VPN warrants further investigation. Secondly, the complex signalling pathways in UPR and the inflammatory response are interrelated during ER stress .…”

“…This VPN model mimics the development of pain in the lower extremities related to acute peripheral arterial ischaemic events followed by reperfusion, which can be encountered in certain clinical situations such as in managing patients with thrombosis formation on atherosclerotic lesions, arterial embolism from the heart or aorta, aortic dissection, and compartment syndrome after extremity vascular injury . VPN induced by IR has been reported to cause hind paw allodynia and hyperalgaesia, impaired motor nerve conduction velocity (MNCV), neuronal oedema and axonal degeneration in the sciatic nerve, and changes to the inflammatory and oxidative markers in serum and the sciatic nerve . Our recent study also revealed that early activation of nuclear factor‐κB (NF‐κB)‐mediated neuroinflammation in the sciatic nerve contributes to the development of allodynia, hyperalgaesia and the debilitating symptoms of VPN …”

Ischemic-reperfusion of unilateral external iliac artery in rat: A new model for vasculitic femoral neuropathy

“…VFN is one kind of the pattern of the ischemic neuropathic pain in post-operative gynecological patients [6]. The mechanism of VFN is primarily due to the release of free radical and various inflammatory mediators in the circulatory system leads to produce the vasculities and vasoconstriction [28]. The acute ischemia induces the structural changes; axonal degeneration subsequently enhances the axonal demyelination [38].…”

“…These mediators induce the structural and functional changes of neuronal cytoskeleton protein [10,29]. In addition, accumulation of cytosolic calcium is responsible for induction of neurodegeneration via m-calpain activation [27][28]. In I/R conditions, the calcium accumulation raises and it enhances the pro-inflammatory cytokine synthesis [15].…”

Investigation of the role of non-selective calcium channel blocker (flunarizine) on cerebral ischemic–reperfusion associated cognitive dysfunction in aged mice

“…Subsequently, it has further altered in various cellular events like lipid peroxidation, accumulation of intracellular calcium ion levels and expression of pro-apoptotic & pro-inflammatory protein (Atif et al, 2009;Lam et al, 2013). The Similar molecular mechanism is explored by various researchers in different organs including brain by applying I/R event (Don et al, 2014;Kao et al, 2011;Muthuraman et al, 2012). In the present study, we have also shown a rise in TBARS (a marker of lipid peroxidation), total calcium (a marker of calcium dys-homeostasis) and decrease in GSH (a marker of endogenous anti-oxidant) levels.…”