Pharmacological evaluation of methanolic leaf extract of Swietenia mahagoni on acrylamide-induced neuropathic pain in rats

Abstract

The present study was designed to investigate the antinociceptive effects of methanolic leaf extract of Swietenia mahagoni (MESM) on acrylamide-induced painful neuropathy in rats. The intraperitoneal administration of acrylamide (30 mg/kg; for 24 consecutive days) has been employed for the induction of painful neuropathy. Acrylamide induced nociceptive pain sensitive changes, which have been assessed by hot plate, Von Frey Hair, and tail immersion tests at different time intervals, that is, 0, 6, 12, 18, and 24th day. Furthermore, the biochemical changes, that is, thiobarbituric acid-reactive substances, reduced glutathione, and total calcium levels have been estimated in sciatic nerve tissue on 24th day and histopathological changes have been observed in sciatic nerve tissue sample. MESM and pregabalin have been administered for 14 consecutive days before 1 h of the each acrylamide injection. Administration of acrylamide resulted in significant changes in behavioral and biochemical parameters. Pretreatment of MESM ameliorated acrylamide-induced behavioral, biochemical, and histopathological changes in a dose-dependent manner, which is similar to that of pregabalin-pretreated group. These findings suggested that the neuroprotective effect of S. mahagoni may be due to its potential of antioxidative, calcium channel modulatory, and neuroprotective action.

The Effect of Anakinra on Acrylamide-induced Peripheral Neuropathy and Neuropathic Pain in Rats

“…Thus, the paw pain threshold of acrylamidetreated rats in the present study was significantly reduced, indicating an impairment in the nociceptive system. The current findings are also in line with the results of a rat study by Vanitha et al (2015), in which the intraperitoneal administration of acrylamide at a dose of 30 mg/kg for 24 days resulted in sciatic neuropathy manifested in the development of thermal hyperalgesia and mechanical allodynia with a decreased hind paw pain threshold. Similarly, Ling et al (2005) demonstrated that low doses of acrylamide (max, 30 mg/kg/day) and a cumulative dose (<250 mg/kg) that did not cause motor dysfunction led to mechanical and thermal allodynia and hyperalgesia.…”

“…Furthermore, proinf lammatory cytokines have been suggested to play a role in the pathogenesis of acrylamide neuropathy as well as reactive oxygen species (ROS) and oxidant products (Yan et al, 2019;Elblehi, El Euony, El-Sayed, 2020). Moreover, Vanitha et al (2015) showed that acrylamiderelated neuropathic pain and damage were reduced with antioxidant treatment. Goudarzi et al (2019) found that ellagic acid protected nerve tissue from the acrylamide oxidative and proinflammatory damage by inhibiting the acrylamide-induced increase of oxidants, tumor necrosis factor (TNF-α), and interleukin-1 beta (IL-1β) in the cerebral cortex.…”

Ameliorative effect of gallic acid in paclitaxel-induced neuropathic pain in mice

“…Our recent findings revealed that alteration of a neuronal microvascular system is primary cardinal signs for the damage and degeneration of the nervous system [[68], [69], [70]]. Furthermore, some of our studies and other laboratory reports recommended that plant extracts and nutritional products of Acorus calamus [51,70], Butea monosperma [71], Swietenia mahagoni [72], Ocimum sanctum [73] and Vernonia cinerea [74] mitigate neuropathic pain symptoms. Phytoconstituents like puerarin [75], bulleyaconitine A [76], thymoquinone, epigallocatechin gallate, lycopene and resveratrol [17] produced an anti-neuralgic effect.…”

Histopathological Study of Protective Effects of Honey on Subacute Toxicity of Acrylamide-Induced Tissue Lesions in Rats’ Brain and Liver

“…It also leads to an increase in the vulnerability of cell membrane and cellular damage and it will eventually lead to neurodegenerative lesions in the brain [14]. Acrylamide induces the oxidative stress associated with enhancement of neuronal intracellular calcium ion concentration along with neurodegeneration [28].…”