title: Neuroprotective and antioxidative effect of cactus polysaccharides in vivo and in vitro.
abstract: Cactus polysaccharides (CP), some of the active components in Opuntia dillenii Haw have been reported to display neuroprotective effects in rat brain slices. In the present study, we investigated the neuroprotective properties of CP and their potential mechanisms on brain ischemia-reperfusion injury in rats, and on oxidative stress-induced damage in PC12 cells. Male Sprague-Dawley rats with ischemia following middle cerebral artery occlusion and reperfusion were investigated. CP (200 mg/kg) significantly decreased the neurological deficit score, reduced infarct volume, decreased neuronal loss in cerebral cortex, and remarkably reduced the protein synthesis of inducible nitric oxide synthase which were induced by ischemia and reperfusion. Otherwise, the protective effect of CP was confirmed in in vitro study. CP protected PC12 cells against hydrogen peroxide (H(2)O(2)) insult. Pretreatment with CP prior to H(2)O(2) exposure significantly elevated cell viability, reduced H(2)O(2)-induced apoptosis, and decreased both intracellular and total accumulation of reactive oxygen species (ROS) production. Furthermore, CP also reversed the upregulation of Bax/Bcl-2 mRNA ratio, the downstream cascade following ROS. These results suggest that CP may be a candidate compound for the treatment of ischemia and oxidative stress-induced neurodegenerative disease.
authors.affiliation: Department of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology, Hangkong Road 13#, 430030, Wuhan, People's Republic of China. huangxj554@sohu.com
authors.forename: Xianju
authors.initials: X
authors.lastname: Huang
authors.forename: Qin
authors.initials: Q
authors.lastname: Li
authors.forename: Huige
authors.initials: H
authors.lastname: Li
authors.forename: Lianjun
authors.initials: L
authors.lastname: Guo
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects / Q000235:genetics; D029421:Cactaceae / Q000737:chemistry*; D002470:Cell Survival / Q000187:drug effects; D002540:Cerebral Cortex / Q000187:drug effects / Q000201:enzymology / Q000473:pathology; D002544:Cerebral Infarction / Q000150:complications / Q000473:pathology; D005786:Gene Expression Regulation / Q000187:drug effects; D006861:Hydrogen Peroxide / Q000494:pharmacology; D020244:Infarction, Middle Cerebral Artery / Q000150:complications / Q000473:pathology; D042541:Intracellular Space / Q000187:drug effects / Q000378:metabolism; D008297:Male; D009474:Neurons / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D018696:Neuroprotective Agents / Q000494:pharmacology*; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D016716:PC12 Cells; D011134:Polysaccharides / Q000494:pharmacology*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000150:complications; D051028:bcl-2-Associated X Protein / Q000235:genetics / Q000378:metabolism
chemical_list: D000975:Antioxidants; D018696:Neuroprotective Agents; D011134:Polysaccharides; D012333:RNA, Messenger; D051028:bcl-2-Associated X Protein; D006861:Hydrogen Peroxide; D052247:Nitric Oxide Synthase Type II