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 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.
Department of Pharmaceutical Sciences, Saurashtra University, Rajkot 360 005, Gujarat, India. Electronic address: sharmatejas87@gmail.com.
Tejas
T
Sharma
Department of Pharmaceutical Sciences, Saurashtra University, Rajkot 360 005, Gujarat, India. Electronic address: vishal.airao@gmail.com.
Vishal
V
Airao
Department of Pharmaceutical Sciences, Saurashtra University, Rajkot 360 005, Gujarat, India. Electronic address: nimesh.panara@yahoo.in.
Nimesh
N
Panara
Department of Pharmaceutical Sciences, Saurashtra University, Rajkot 360 005, Gujarat, India. Electronic address: devvaishnav@gmail.com.
Devendra
D
Vaishnav
Department of Pharmaceutical Sciences, Saurashtra University, Rajkot 360 005, Gujarat, India. Electronic address: vishwash811@yahoo.co.in.
Vishavas
V
Ranpariya
Department of Pharmaceutical Sciences, Saurashtra University, Rajkot 360 005, Gujarat, India. Electronic address: navin_sheth@yahoo.com.
Navin
N
Sheth
Department of Pharmaceutical Sciences, Saurashtra University, Rajkot 360 005, Gujarat, India. Electronic address: parmarsachin@rediffmail.com.
Sachin
S
Parmar
D000818:Animals; D000975:Antioxidants / Q000009:adverse effects / Q000494:pharmacology*; D001921:Brain / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism / Q000473:pathology; D007928:Lethal Dose 50; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D018696:Neuroprotective Agents / Q000009:adverse effects / Q000494:pharmacology*; D009569:Nitric Oxide / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000201:enzymology / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D012991:Solanaceous Alkaloids / Q000009:adverse effects / Q000494:pharmacology*
D000975:Antioxidants; D018696:Neuroprotective Agents; D012991:Solanaceous Alkaloids; D009569:Nitric Oxide; C012037:solasodine
(±)-epinephrine (PubChem CID:5815); 2,3,5-triphenyltetrazolium chloride (PubChem CID:9283); 2-thiobarbituric acid (PubChem CID:2723628); 5-5-dithiobis (2-nitrobenzoic acid) (PubChem CID:6254); Antioxidants; Global ischemia; Glutathione (PubChem CID:124886); Hydrogen peroxide (PubChem CID:784); Naphthyl-ethylenediamine (PubChem CID:15106); Neuroprotection; Oxidative stress; Solasodine; Stroke; Sulfanilamide (PubChem CID:5333); Trichloroacetic Acid (PubChem CID:6421)