Rosa damascena Mill. L. attenuates myocardial lysosomal membrane destabilization in isoproterenol induced oxidative stress

Pullaiah, Chitikela P; Kumar, G V Narasimha; Jyothsna, K.; Thyagaraju, K.; Nelson, Vinod K.; Reddy, G. Dayanand

doi:10.1007/s13596-017-0290-x

Cited by 10 publications

(8 citation statements)

References 17 publications

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“…Hence, signi cant attention has been raised on the involvement of lysosomal enzymes in myocardial damage. From our previous report it was observed that, administration of the ISO to the rats causes a signi cant elevation in the activities of the lysosomal enzymes [30]. In the present study same effect observed.…”

Section: Discussionsupporting

confidence: 89%

“…Anti-oxidant enzymes such as catalase, superoxide dismutase (SOD), glutathione peroxidase and glutathione-S transferase (GSH) are the rst line of cellular defense against oxidative injury by superoxide anion radical and H 2 O 2 before interacting to form the more reactive hydroxyl radical [28]. Auto-oxidation of ISO produces highly cytotoxic free radicals like quinines which in addition with superoxide anion and potent hydroxyl radicals damages the polyunsaturated fatty acids of myocardial membrane [29,30]. The elevation of these free radicals brings an imbalance between tissue bound cellular scavenging enzymes like SOD, GSH and Catalase and lipid peroxidase [31].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Exploring Cardioprotective Potential of Esculetin Against Isoproterenol Induced Myocardial Infarction in Rats: In Vivo and in Vitro Evidence

Pullaiah

Nelson²,

Sushma

et al. 2021

Preprint

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BackgroundEsculetin is a natural coumarin derivative from various plants with multiple pharmacological effects. Hence, the present study was undertaken to explore the cardio protective potential of esculetin against isoproterenol induced myocardial toxicity in rats. Methods The treatment schedule was fixed for 28 days and the rats were divided into five groups of six each. Rats of group I received the normal saline and served as normal control, group II was received ISO (100mg/kg body weight) for last two consecutive days of the study and served as disease control. Groups III and IV received esculetin 10 and 20 mg/kg body weight respectively once a day per oral for 28 days along with ISO for last two consecutive days of the study. Cardiac biomarkers such as CK-MB and LDH, membrane bound Na+ /K+ ATPases activity, myocardial lysosomal enzymes activity and tissue antioxidants status were estimated in the heart tissue samples. The histopathological changes in the myocardium were also assessed. Further, DPPH assay was done to evaluate the free radicals scavenging potential of esculetin. Cytoxicity assay, intracellular ROS levels by DCFDA assay and m-RNA expression of TNF-α, IL-6 and NF-κB by quantitative RT-PCR in H9c2 cell lines.ResultsThe increased levels of CK-MB, LDH, LPO, myocardial lysosomal enzymes and membrane bound Na+ /K+ ATPase levels by ISO administration was significantly increased with concomitant decrease in tissue antioxidant enzymes such as GSH, Catalase, and SOD. Pre-treatment with esculetin for 28 days has significantly decreased the levels of cardiac bio-markers, lysosomal enzymes, membrane bound Na+ /K+ ATPase levels as well as Lipid peroxides which is in contrary to the ISO group. Amelioration of the antioxidant levels were also found in esculetin treated groups. Histopathological examination of heart reveals that myocardial degeneration, mononuclear cell infiltration was noticed in ISO treated rats, whereas the same was restored with esculetin treatment. In H9C2 cell lines esculetin could effectively reduced intracellular ROS inhibition and m-RNA expression of pro-inflammatory cytokines including TNF-α, IL-6 and NF-κB to prevent apoptosis or cell necrosis. Conclusion The study provides the evidence of cardioprotective potentials of esculetin against isoproterenol induced myocardial infarction by antioxidant and myocardial membrane stabilization along with in vitro protection from arsenic induced ROS cell necrosis or apoptosis in H9C2 cells.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Exploring Cardioprotective Potential of Esculetin Against Isoproterenol Induced Myocardial Infarction in Rats: In Vivo and in Vitro Evidence

Pullaiah

Nelson²,

Sushma

et al. 2021

Preprint

View full text Add to dashboard Cite

show abstract

“…Hence, significant attention has been raised on the involvement of lysosomal enzymes in myocardial damage. From our previous report it was observed that, administration of the ISO to the rats causes a significant elevation in the activities of the lysosomal enzymes [30]. In the present study same effect observed.…”

Section: Discussionsupporting

confidence: 89%

“…Anti-oxidant enzymes such as catalase, superoxide dismutase (SOD), glutathione peroxidase and glutathione-S transferase (GSH) are the first line of cellular defense against oxidative injury by superoxide anion radical and H 2 O 2 before interacting to form the more reactive hydroxyl radical [28]. Auto-oxidation of ISO produces highly cytotoxic free radicals like quinines which in addition with superoxide anion and potent hydroxyl radicals damages the polyunsaturated fatty acids of myocardial membrane [29,30]. The elevation of these free radicals brings an imbalance between tissue bound cellular scavenging enzymes like SOD, GSH and Catalase and lipid peroxidase [31].…”

Section: Discussionmentioning

confidence: 99%

Exploring cardioprotective potential of esculetin against isoproterenol induced myocardial toxicity in rats: in vivo and in vitro evidence

Pullaiah

Nelson

Rayapu

et al. 2021

BMC Pharmacol Toxicol

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Background Esculetin is a natural coumarin derivative from various plants with multiple pharmacological effects. Hence, the present study was undertaken to explore the cardio protective potential of esculetin against isoproterenol induced myocardial toxicity in rats. Methods The treatment schedule was fixed for 28 days and the rats were divided into five groups of six each. Rats of group I received the normal saline and served as normal control, group II was received ISO (100 mg/kg body weight) for last two consecutive days of the study and served as disease control. Groups III and IV received esculetin 10 and 20 mg/kg body weight respectively once a day per oral for 28 days along with ISO for last two consecutive days of the study. Cardiac biomarkers such as CK-MB and LDH, membrane bound Na+ /K+ ATPases activity, myocardial lysosomal enzymes activity and tissue antioxidants status were estimated in the heart tissue samples. The histopathological changes in the myocardium were also assessed. Further, DPPH assay was done to evaluate the free radicals scavenging potential of esculetin. Cytoxicity assay, intracellular ROS levels by DCFDA assay and m-RNA expression of TNF-α, IL-6 and NF-κB by quantitative RT-PCR in H9c2 cell lines. Results The increased levels of CK-MB, LDH, LPO, myocardial lysosomal enzymes and membrane bound Na+ /K+ ATPase levels by ISO administration was significantly increased with concomitant decrease in tissue antioxidant enzymes such as GSH, Catalase, and SOD. Pre-treatment with esculetin for 28 days has significantly decreased the levels of cardiac bio-markers, lysosomal enzymes, membrane bound Na+ /K+ ATPase levels as well as Lipid peroxides which is in contrary to the ISO group. Amelioration of the antioxidant levels were also found in esculetin treated groups. Histopathological examination of heart reveals that myocardial degeneration, mononuclear cell infiltration was noticed in ISO treated rats, whereas the same was restored with esculetin treatment. In H9C2 cell lines esculetin could effectively reduced intracellular ROS inhibition and m-RNA expression of pro-inflammatory cytokines including TNF-α, IL-6 and NF-κB to prevent apoptosis or cell necrosis. Conclusion The study provides the evidence of cardioprotective potentials of esculetin against isoproterenol induced myocardial infarction by antioxidant and myocardial membrane stabilization along with in vitro protection from arsenic induced ROS cell necrosis or apoptosis in H9C2 cells.

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“…Rats were pretreated with MP (150 mg/kg, p.o) three times per week on alternating days for 2 weeks and then injected with 2 consecutive doses of ISO (85 mg/kg, s.c) on the 13th and 14th days; data are presented as mean ± SD (n = 7); a or b: significantly different from control or ISO groups respectively at P < 0.05 using one-way ANOVA followed by Tukey as a post hoc test. MP methyl palmitate, ISO isoproterenol, MDA malondialdehyde, GSH reduced glutathione, SOD superoxide dismutase Catecholamines produce excessive amounts of free radicals inducing myocardial injury, due to their transformation into aminochromes, which undergo redox cycling in mitochondria resulting in the production of profuse amounts of oxygen-derived free radicals leading to loss of myocardial membranes function and integrity [40]. Herein the present study, ISO-intoxicated rats exhibited severe oxidative damage evidenced by the significant elevation in cardiac content of malondialdehyde (MDA), the lipid peroxidation product, and the marked reduction of the antioxidant defenses reduced glutathione (GSH) and superoxide dismutase (SOD) enzyme.…”

Section: Discussionmentioning

confidence: 99%

Putative anti-inflammatory, antioxidant, and anti-apoptotic roles of the natural tissue guardian methyl palmitate against isoproterenol-induced myocardial injury in rats

et al. 2020

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Background Myocardial injury is considered as a worldwide main cause of morbidity and mortality. The present study aimed to investigate the probable cardioprotective activity of the naturally occurring endogenous fatty acid ester methyl palmitate (MP) against isoproterenol (ISO)-induced myocardial injury in rats and the possible underlying molecular mechanisms. The study was carried out in two consecutive sets of experiments; the first set screened the cardioprotective dose of MP in ISO-intoxicated rats. In the second set, forty male Sprague Dawley rats received either MP (150 mg/kg, p.o) three times/week for 2 weeks and/or 2 consecutive doses of ISO separated by 24 h (85 mg/kg, s.c) on the 13th and 14th days. Different cardiotoxicity and oxidative stress markers were assessed. Furthermore, endothelial nitric oxide synthase (eNOS) levels were determined. For detection of apoptosis, Bax, Bcl-2, and caspase 3 were estimated. To assess inflammation, toll-like receptor 4 (TLR-4) and tumor necrosis factor-alpha (TNF-α) were measured using ELISA. Meanwhile, nuclear factor kappa B (NF-kB) and cyclooxygenase-2 (COX-2) were detected immunohistochemically. Results Pretreatment with MP significantly ameliorated the cardiotoxicity and oxidative stress markers. It also markedly elevated eNOS content, decreased apoptotic marker expression, and mitigated TLR-4 activation and other inflammatory markers. Electrocardiography and histopathological examination also confirmed the cardioprotective effect of MP. Conclusion The findings of this study indicated that MP possesses a potent cardioprotective activity against ISO-induced myocardial injury through its significant antioxidant, anti-apoptotic, anti-inflammatory, and vasodilatation activities. Graphical abstract

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Rosa damascena Mill. L. attenuates myocardial lysosomal membrane destabilization in isoproterenol induced oxidative stress

Cited by 10 publications

References 17 publications

Exploring Cardioprotective Potential of Esculetin Against Isoproterenol Induced Myocardial Infarction in Rats: In Vivo and in Vitro Evidence

Exploring Cardioprotective Potential of Esculetin Against Isoproterenol Induced Myocardial Infarction in Rats: In Vivo and in Vitro Evidence

Exploring cardioprotective potential of esculetin against isoproterenol induced myocardial toxicity in rats: in vivo and in vitro evidence

Putative anti-inflammatory, antioxidant, and anti-apoptotic roles of the natural tissue guardian methyl palmitate against isoproterenol-induced myocardial injury in rats

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