<mets:mets OBJID="eprint_3402" LABEL="Eprints Item" xsi:schemaLocation="http://www.loc.gov/METS/ http://www.loc.gov/standards/mets/mets.xsd http://www.loc.gov/mods/v3 http://www.loc.gov/standards/mods/v3/mods-3-3.xsd" xmlns:mets="http://www.loc.gov/METS/" xmlns:mods="http://www.loc.gov/mods/v3" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance"><mets:metsHdr CREATEDATE="2026-05-03T21:26:14Z"><mets:agent ROLE="CUSTODIAN" TYPE="ORGANIZATION"><mets:name>open</mets:name></mets:agent></mets:metsHdr><mets:dmdSec ID="DMD_eprint_3402_mods"><mets:mdWrap MDTYPE="MODS"><mets:xmlData><mods:titleInfo><mods:title>Indian Ginseng (Withania somnifera) supplementation ameliorates oxidative stress and mitochondrial dysfunctions in experimental model of stroke</mods:title></mods:titleInfo><mods:name type="personal"><mods:namePart type="given">Abhilasha</mods:namePart><mods:namePart type="family">Sood</mods:namePart><mods:role><mods:roleTerm type="text">author</mods:roleTerm></mods:role></mods:name><mods:name type="personal"><mods:namePart type="given">Arpit</mods:namePart><mods:namePart type="family">Mehrotra</mods:namePart><mods:role><mods:roleTerm type="text">author</mods:roleTerm></mods:role></mods:name><mods:name type="personal"><mods:namePart type="given">Devinder K</mods:namePart><mods:namePart type="family">Dhawan</mods:namePart><mods:role><mods:roleTerm type="text">author</mods:roleTerm></mods:role></mods:name><mods:name type="personal"><mods:namePart type="given">Rajat</mods:namePart><mods:namePart type="family">Sandhir</mods:namePart><mods:role><mods:roleTerm type="text">author</mods:roleTerm></mods:role></mods:name><mods:abstract>Stroke is an increasingly prevalent clinical condition and second leading cause of death globally. The present study evaluated the therapeutic potential of Indian Ginseng, also known as Withania somnifera (WS), supplementation on middle cerebral artery occlusion (MCAO) induced mitochondrial dysfunctions in experimental model of ischemic stroke. Stroke was induced in animals by occluding the middle cerebral artery, followed by reperfusion injury. Ischemia reperfusion injury resulted in increased oxidative stress indicated by increased reactive oxygen species and protein carbonyl levels; compromised antioxidant system; in terms of reduced superoxide dismutase and catalase activity, along with reduction in GSH levels and the redox ratio, impaired mitochondrial functions and enhanced expression of apoptosis markers. Ischemia reperfusion injury induced mitochondrial dysfunctions in terms of (i) reduced activity of the mitochondrial respiratory chain enzymes, (ii) reduced histochemical staining of complex-II and IV, (iii) reduced in-gel activity of mitochondrial complex-I to V, (iv) mitochondrial structural changes in terms of increased mitochondrial swelling, reduced mitochondrial membrane potential and ultrastructural changes. Additionally, an increase in the activity of caspase-3 and caspase-9 was also observed, along with altered expression of apoptotic proteins Bcl-2 and Bax in MCAO animals. MCAO animals also showed significant impairment in cognitive functions assessed using Y maze test. WS pre-supplementation, on the other hand ameliorated MCAO induced oxidative stress, mitochondrial dysfunctions, apoptosis and cognitive impairments. The results show protective effect of WS pre-supplementation in ischemic stroke and are suggestive of its potential application in stroke management.</mods:abstract><mods:classification authority="lcc">QR Microbiology</mods:classification><mods:originInfo><mods:dateIssued encoding="iso8061">2023-06-01</mods:dateIssued></mods:originInfo><mods:originInfo><mods:publisher>Springer Science and Business Media LLC</mods:publisher></mods:originInfo><mods:genre>Article</mods:genre></mets:xmlData></mets:mdWrap></mets:dmdSec><mets:amdSec ID="TMD_eprint_3402"><mets:rightsMD ID="rights_eprint_3402_mods"><mets:mdWrap MDTYPE="MODS"><mets:xmlData><mods:useAndReproduction>
<p xmlns="http://www.w3.org/1999/xhtml"><strong>For work being deposited by its own author:</strong> 
In self-archiving this collection of files and associated bibliographic 
metadata, I grant open the right to store 
them and to make them permanently available publicly for free on-line. 
I declare that this material is my own intellectual property and I 
understand that open does not assume any 
responsibility if there is any breach of copyright in distributing these 
files or metadata. (All authors are urged to prominently assert their 
copyright on the title page of their work.)</p>

<p xmlns="http://www.w3.org/1999/xhtml"><strong>For work being deposited by someone other than its 
author:</strong> I hereby declare that the collection of files and 
associated bibliographic metadata that I am archiving at 
open) is in the public domain. If this is 
not the case, I accept full responsibility for any breach of copyright 
that distributing these files or metadata may entail.</p>

<p xmlns="http://www.w3.org/1999/xhtml">Clicking on the deposit button indicates your agreement to these 
terms.</p>
    </mods:useAndReproduction></mets:xmlData></mets:mdWrap></mets:rightsMD></mets:amdSec><mets:fileSec></mets:fileSec><mets:structMap><mets:div DMDID="DMD_eprint_3402_mods" ADMID="TMD_eprint_3402"></mets:div></mets:structMap></mets:mets>