Affiliations 

  • 1 Department of Pharmacology, Chaudhary Devi Lal College of Pharmacy, BD Sharma University of Health Science, Yamuna Nagar, Yamuna Nagar-135003, Haryana, India
  • 2 Department of Pharmacology and Toxicology, Akal College of Pharmacy & Technical Education, Punjab Technical University (Jalandhar), Mastuana Sahib, Sangrur-147001, Punjab, India
Toxicol Rep, 2019;6:505-513.
PMID: 31211096 DOI: 10.1016/j.toxrep.2019.06.001

Abstract

The present study has been investigated the role of gallic acid (GA) in paclitaxel-induced neuropathic pain. The neuropathic pain was developed with paclitaxel (PT: 2 mg/kg, i.p.) administration in mice. GA (20 and 40 mg/kg) and pregabalin (PreG: 5 mg/kg) were administered intravenously for 10 consecutive days. The neuralgic sensations were investigated by assessing various pain tests like acetone drop, pinprick, plantar, tail flick, and tail pinch test. Mice pain behaviors were evaluated on 0, 4th, 8th, 12th and 16th days. The levels of sciatic nerve thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH), superoxide anion, calcium, myeloperoxidase (MPO), and TNF-α were estimated. Treatment of GA and PreG attenuate PT induced thermal &mechanical hyperalgesia and allodynia symptoms along with the reduction of TBARS, total calcium, TNF-α, superoxide anion, and MPO activity levels; and decreased GSH level. Therefore, it has been concluded that GA has potential neuroprotective actions against PT induced neuropathic pain due to it's anti-oxidant, anti-inflammation and regulation of intracellular calcium ion concentration.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.