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        <identifier>oai:figshare.com:article/33786109</identifier>
        <datestamp>2026-09-15T10:33:54Z</datestamp>
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          <dc:title>Table 1_Effects of candesartan on cellular redox status and bioenergetics of cardiac tissue in normal and chronically stressed rats.docx</dc:title>
          <dc:creator>Mahmoud M. A. Abulmeaty (12451461)</dc:creator>
          <dc:creator>Hazem K. Ghneim (13928784)</dc:creator>
          <dc:creator>Dara Aldisi (12451464)</dc:creator>
          <dc:creator>Reham M. Wahid (24927067)</dc:creator>
          <dc:creator>Wesam M. R. Ashour (24927070)</dc:creator>
          <dc:creator>John P. Giesy (302766)</dc:creator>
          <dc:creator>Mourad A. M. Aboul-Soud (13928793)</dc:creator>
          <dc:subject>Pharmacology</dc:subject>
          <dc:subject>angiotensin receptor blocker</dc:subject>
          <dc:subject>candesartan</dc:subject>
          <dc:subject>cellular redox state</dc:subject>
          <dc:subject>mitochondrial bioenergetics</dc:subject>
          <dc:subject>myocardial tissue</dc:subject>
          <dc:subject>oxidative stress</dc:subject>
          <dc:subject>unpredictable chronic mild stress</dc:subject>
          <dc:description>Background&lt;p&gt;Studies of redox status and bioenergetics in cardiac tissue during unpredictable chronic mild stress (UCMS) are scarce. The present study examined the effect of candesartan, an angiotensin II type 1 receptor (AT1R) blocker primarily used to treat hypertension and congestive heart failure, on the antioxidant capacity and energy homeostasis of cardiac tissue in UCMS-subjected rats.&lt;/p&gt;Methods&lt;p&gt;Forty-eight male Wistar rats were randomly assigned to four groups (n = 12/group): undosed normal controls (NC), UCMS-subjected rats (UCMS), unstressed candesartan-treated rats (Can), and stressed candesartan-treated rats (UCMS + Can). Enzyme activities and mRNA transcripts of key antioxidant enzymes, tricarboxylic acid cycle enzymes, and respiratory chain complexes were measured in myocardial tissue, together with oxidative-phosphorylation (OXPHOS) markers, redox state, and the energy-homeostasis ratios GSH/GSSG, NAD&lt;sup&gt;+&lt;/sup&gt;/NADH, and ATP/ADP.&lt;/p&gt;Results&lt;p&gt;The UCMS group showed marked elevations in oxidative-stress markers, accompanied by significantly reduced antioxidant enzyme activities and downregulated antioxidant gene expression. In parallel, all TCA-cycle and OXPHOS enzyme activities were significantly decreased, and their relative gene transcripts were markedly downregulated. The cellular GSH/GSSG and ATP/ADP ratios were significantly lowered, whereas the NAD&lt;sup&gt;+&lt;/sup&gt;/NADH ratio was increased. Each of these changes was either fully reversed or significantly attenuated in unstressed and stressed rats receiving candesartan.&lt;/p&gt;Conclusion&lt;p&gt;Candesartan clearly mitigates cellular oxidative stress and the disruption of energy metabolism in the myocardial tissue of UCMS-subjected rats. Because blood pressure, cardiac function and systemic haemodynamics were not measured, these findings should be interpreted as biochemical evidence of a cytoprotective action of AT1R blockade in myocardial tissue, and they provide a preliminary rationale for further evaluation of candesartan in stress-related cardiovascular disorders.&lt;/p&gt;</dc:description>
          <dc:date>2026-09-15T10:33:54Z</dc:date>
          <dc:type>Dataset</dc:type>
          <dc:type>Dataset</dc:type>
          <dc:identifier>10.3389/fphar.2026.1876050.s001</dc:identifier>
          <dc:relation>https://figshare.com/articles/dataset/Table_1_Effects_of_candesartan_on_cellular_redox_status_and_bioenergetics_of_cardiac_tissue_in_normal_and_chronically_stressed_rats_docx/33786109</dc:relation>
          <dc:rights>CC BY 4.0</dc:rights>
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