Lavanya Yaidikar1, Santhrani Thakur2. 1. Division of Pharmacology, Institute of Pharmaceutical Technology, Sri Padmavati Mahila Visvavidyalayam (Women's University), Tirupati, India. 2. Division of Pharmacology, Institute of Pharmaceutical Technology, Sri Padmavati Mahila Visvavidyalayam (Women's University), Tirupati, India. Electronic address: drsanthrani@gmail.com.
Abstract
BACKGROUND: Arjunolic acid (AA), a pentacyclic triterpenoidal saponin of Terminalia arjuna is well recognized for its antioxidant properties. We proposed to evaluate its antioxidant potential against focal cerebral ischemia reperfusion (I/R) injury in rats subjected to middle cerebral artery occlusion (MCAO). METHODS: In the present study, rats were randomly divided into a sham, MCAO, AA (10 and 20mg/kg) treated groups. Rats received their respective treatment orally by gavage for 7 days prior to MCAO. Rats were anaesthetized with ketamine (100mg/kg), xylazine (10mg/kg) and subjected to 2h occlusion and 22h reperfusion. Neurological deficit, brain water content and oxidative stress markers were measured after 22h of reperfusion. RESULTS: Rats pretreated with AA showed significantly reduced neurological deficit score, infarct size. AA prevented neuronal damage induced by I/R by regulating the levels of malondialdehyde (MDA), reduced glutathione (GSH), nitric oxide (NO), protein carbonyl content and mitochondria generated reactive oxygen species. In addition, it also controlled the enzyme activities of Na(+)-K(+) ATPase, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR). CONCLUSIONS: Pre-treatment with AA effectively prevented the cerebral I/R induced oxidative damage by virtue of its antioxidant potential. These results indicate that supplementation of AA may be beneficial in stroke prone population.
BACKGROUND:Arjunolic acid (AA), a pentacyclic triterpenoidalsaponin of Terminalia arjuna is well recognized for its antioxidant properties. We proposed to evaluate its antioxidant potential against focal cerebral ischemia reperfusion (I/R) injury in rats subjected to middle cerebral artery occlusion (MCAO). METHODS: In the present study, rats were randomly divided into a sham, MCAO, AA (10 and 20mg/kg) treated groups. Rats received their respective treatment orally by gavage for 7 days prior to MCAO. Rats were anaesthetized with ketamine (100mg/kg), xylazine (10mg/kg) and subjected to 2h occlusion and 22h reperfusion. Neurological deficit, brain water content and oxidative stress markers were measured after 22h of reperfusion. RESULTS:Rats pretreated with AA showed significantly reduced neurological deficit score, infarct size. AA prevented neuronal damage induced by I/R by regulating the levels of malondialdehyde (MDA), reduced glutathione (GSH), nitric oxide (NO), protein carbonyl content and mitochondria generated reactive oxygen species. In addition, it also controlled the enzyme activities of Na(+)-K(+) ATPase, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR). CONCLUSIONS: Pre-treatment with AA effectively prevented the cerebral I/R induced oxidative damage by virtue of its antioxidant potential. These results indicate that supplementation of AA may be beneficial in stroke prone population.
Authors: Bai Hui Chen; Joon Ha Park; Ji Hyeon Ahn; Jeong Hwi Cho; In Hye Kim; Jae Chul Lee; Moo-Ho Won; Choong-Hyun Lee; In Koo Hwang; Jong-Dai Kim; Il Jun Kang; Jun Hwi Cho; Bich Na Shin; Yang Hee Kim; Yun Lyul Lee; Seung Min Park Journal: Neural Regen Res Date: 2017-02 Impact factor: 5.135