Neuroprotective Effect of Corosolic Acid Against Cerebral Ischemia-Reperfusion Injury in Experimental Rats

J Oleo Sci. 2022 Sep 30;71(10):1501-1510. doi: 10.5650/jos.ess22130. Epub 2022 Sep 9.

Abstract

Several therapeutic approaches were also urgently needed as ischaemic stroke was one of the most common brain disorders. Many phytochemicals have recently been discovered for the advancement of lead-like libraries that are concentrated on the peripheral and central nervous systems. Science does not yet understand how these drugs work, nor do they comprehend their in vivo characteristics. We investigated the potential benefits of corosolic acid (CA) in the treatment of brain injury caused by ischemia/reperfusion (I/R) in adult male Sprague-Dawley rats. Injury occurs after a 2-hour transient occlusion of the posterior cerebral artery and subsequent reperfusion (after 20 hours). Furthermore, the experiment assessed the size of the infarct, the amount of brain water present, as well as the neurofunctional conditions in rats. In the study, several markers of inflammation and cytokines associated with brain injury were measured. The Elisa kit was used in this study to measure the mRNA expression of interleukin-6 (IL-6), interleukin-10 (IL-10), interleukin 1β, TNF-α (tumor necrosis factor), cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), and nitrous oxide (NO). The CA treatment significantly reduced brain water content, brain infarction volume, neurological scores, and Evans blue leakage (p < 0.001 and p < 0.001). Experimental rats were treated with CA after a significantly reduced level of anti-inflammatory, pro-inflammatory, and oxidative stress mediators was noted in their body tissues and serum (p < 0.001). By suppressing inflammatory responses in rats, CA demonstrated anti-inflammatory and neuroprotective properties.

Keywords: antioxidants; corosolic acid; inflammatory cytokines; ischemia/reperfusion (I/R) injury; neuroinflammation.

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / therapeutic use
  • Brain Injuries* / complications
  • Brain Injuries* / drug therapy
  • Brain Ischemia* / drug therapy
  • Brain Ischemia* / metabolism
  • Cyclooxygenase 2 / metabolism
  • Cytokines / metabolism
  • Dinoprostone
  • Evans Blue / therapeutic use
  • Interleukin-10
  • Interleukin-1beta / genetics
  • Interleukin-6 / genetics
  • Male
  • Neuroprotective Agents* / pharmacology
  • Neuroprotective Agents* / therapeutic use
  • Nitrous Oxide / therapeutic use
  • RNA, Messenger
  • Rats
  • Rats, Sprague-Dawley
  • Reperfusion Injury* / drug therapy
  • Reperfusion Injury* / metabolism
  • Stroke* / drug therapy
  • Triterpenes
  • Tumor Necrosis Factor-alpha / metabolism
  • Water

Substances

  • Anti-Inflammatory Agents
  • Cytokines
  • Interleukin-1beta
  • Interleukin-6
  • Neuroprotective Agents
  • RNA, Messenger
  • Triterpenes
  • Tumor Necrosis Factor-alpha
  • Water
  • Interleukin-10
  • Evans Blue
  • corosolic acid
  • Cyclooxygenase 2
  • Nitrous Oxide
  • Dinoprostone