Solasodine protects rat brain against ischemia/reperfusion injury through its antioxidant activity

Ischemic stroke is the second leading cause of death worldwide. The major limitation of stroke management is the lack of clinically effective therapy. Antioxidants have been demonstrated as potent neuroprotective agents by enhancing the defense mechanism(s), whereas reducing the oxidative stress in...

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Bibliographic Details
Published in:European journal of pharmacology 2014-02, Vol.725, p.40-46
Main Authors: Sharma, Tejas, Airao, Vishal, Panara, Nimesh, Vaishnav, Devendra, Ranpariya, Vishavas, Sheth, Navin, Parmar, Sachin
Format: Article
Language:English
Subjects:
Animals
Antioxidants
Antioxidants - adverse effects
Antioxidants - pharmacology
Brain - drug effects
Brain - enzymology
Brain - metabolism
Brain - pathology
Global ischemia
Lethal Dose 50
Lipid Peroxidation - drug effects
Male
Neuroprotection
Neuroprotective Agents - adverse effects
Neuroprotective Agents - pharmacology
Nitric Oxide - metabolism
Oxidative stress
Rats
Rats, Wistar
Reperfusion Injury - enzymology
Reperfusion Injury - metabolism
Reperfusion Injury - pathology
Reperfusion Injury - prevention & control
Solanaceous Alkaloids - adverse effects
Solanaceous Alkaloids - pharmacology
Solanum
Solasodine
Stroke
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Summary:Ischemic stroke is the second leading cause of death worldwide. The major limitation of stroke management is the lack of clinically effective therapy. Antioxidants have been demonstrated as potent neuroprotective agents by enhancing the defense mechanism(s), whereas reducing the oxidative stress in the ischemic stroke models. In the present study, we evaluated neuroprotective potential of solasodine, an antioxidant glycoalkaloid of Solanum species, against global model of ischemia in rats. Ischemia/reperfusion (I/R)-injury produced marked elevation in lipid peroxidation (LPO) and nitric oxide (NO), whereas superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH) levels were decreased in experimental animals. Prior administration of solasodine (100 and 200mg/kg, p.o.) significantly heightened SOD, CAT, GSH and total thiols, whereas reduced LPO and NO levels in the brain. Interestingly, brain coronal sectioning and histopathology studies revealed a marked reversal of I/R-provoked neuronal damage in the solasodine treatment groups. Taken together, our study, for the first time, demonstrates neuroprotective potential of solasodine against global ischemia-induced cerebral injury in experimental rats. We propose that the neuroprotection offered by solasodine could be attributed, at least in part, to its anti-oxidant property. [Display omitted]
ISSN:0014-2999
1879-0712
DOI:10.1016/j.ejphar.2014.01.005