Attenuation of ROS-mediated myocardial ischemia–reperfusion injury by morin via regulation of RISK/SAPK pathways

Verma, Vipin; Malik, Salma; Mutneja, Ekta; Sahu, Anil Kumar; Bhatia, Jagriti; Arya, Dharamvir Singh

doi:10.1007/s43440-019-00011-2

Cited by 16 publications

(7 citation statements)

References 42 publications

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“…This indicated apoptosis induced by CIS via redox imbalance and proinflammation. Among caspases, caspase-3 is the main executor of apoptosis triggering enzyme degradation, protein denaturation and cell death [48,49]. Our findings herein confirmed suggestions in existing literatures that cytotoxic apoptosis and inflammatory responses play a mechanistic role in the pathophysiology of CIS-induced organ toxicity [29,46,50,51].…”

Section: Discussionsupporting

confidence: 89%

Tiliacora triandra attenuates cisplatin triggered hepatorenal and testicular toxicity in rats by modulating oxidative inflammation, apoptosis and endocrine deficit

Zhang¹,

Peng²,

Wang³

et al. 2022

Front. Biosci. (Landmark Ed)

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Purpose: Cisplatin (CIS) is a platinum based anticancer drug that has demonstrated significant efficacy against various types of cancers. Unfortunately, this drug is also famous for its severe side effects on delicate organs. Herein this study examined the hepatorenal and testicular protective effects of TiTE against CIS-induced hepatorenal and testicular insults. Methods: Rats were administered with TiTE (250 and 500 mg/kg body weight) for 4 weeks, while a single dose of CIS (2.5 mg/kg body weight) was injected once per week from week 2 to week 4. Results: Treatment with TITE significantly attenuated CIS-induced increases in serum creatinine, blood urea nitrogen (BUN), uric acid, alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Furthermore, TiTE treatment also decreased oxidative stress (MDA) inflammations (TNF-α, IL-1β, IL-6, NF-κB) and apoptosis (caspase-3 activity) and restored hepatorenal and testicular antioxidant defense (SOD, CAT and GPx) in CIS treated rats. Additionally, the TiTE improved sperm count, motility and viability, and ameliorated the reduced serum levels of testosterone, follicle stimulating hormone (FSH) and luteinizing hormone (LH) in CIS-injected rats. TiTE also curtailed hepatorenal and testicular histological changes in CIS treated rats. Conclusion: The findings from the study indicated that TiTE displayed hepatorenal and testicular protective effects via inhibition of oxidative stress-mediated inflammation and endocrine imbalance in rats.

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Section: Discussionsupporting

confidence: 89%

Tiliacora triandra attenuates cisplatin triggered hepatorenal and testicular toxicity in rats by modulating oxidative inflammation, apoptosis and endocrine deficit

Zhang¹,

Peng²,

Wang³

et al. 2022

Front. Biosci. (Landmark Ed)

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“…During reperfusion, apoptosis is promoted by MAPK by activating Bax (proapoptotic protein), and this cardiac damage is stopped by the upregulation of the pro‐survival MAPK, ERK1/ERK2. [ 27 ] In our study, AZL modulated apoptosis and MAPK to a lesser extent in comparison to telmisartan through both ARBs exerted antiapoptotic and beneficial MAPK‐modulating effects. The aforementioned effects seem to be a result of PPAR‐γ‐mediated suppression of oxidative stress and inflammation which is in keeping with previous studies.…”

Section: Discussionmentioning

confidence: 58%

Cardioprotective effects of azilsartan compared with that of telmisartan on an in vivo model of myocardial ischemia‐reperfusion injury

Garg

Khan

Malhotra

et al. 2021

J Biochem & Molecular Tox

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Azilsartan is found to be more potent than other angiotensin receptor blockers in reducing blood pressure. However, its effect on the heart following myocardial infarction remains to be established. For the first time, we investigated the peroxisome proliferator-activated receptor-γ (PPAR-γ) agonistic and cardioprotective properties of azilsartan. Computational modeling studies of interactions between azilsartan and PPAR-γ revealed azilsartan as an agonist of PPAR-γ and showed the mechanism of azilsartan in cardioprotection. Our study compared the cardioprotective potential of telmisartan to that of azilsartan in a murine model of myocardial ischemia-reperfusion injury by comparing their antioxidant, ant apoptotic, antiinflammatory, mitogen-activated protein kinase (MAPK)-modulating ability, and PPAR-γ agonistic activity. Male Wistar rats were grouped into four to receive vehicle (dimethyl sulfoxide [0.05%] 2 ml/kg) telmisartan (10 mg/kg p.o.), azilsartan (10 mg/kg p.o.) or azilsartan with specific PPAR-γ blocker, GW 9662 for 28 days.Ischemia was induced for 45 min on the 29th day followed by 60 min of reperfusion.Telmisartan and azilsartan pretreatment significantly nearly normalized cardiac parameters and preserved structural changes. Both drugs inhibited oxidative burst, inflammation, as well as cell death by modulating apoptotic protein expression along with reduction in 4′,6-diamidino-2-phenylindole/terminal deoxynucleotidyl transferase dUTP nick end labeling-positive cells. An increment in pro-survival kinase ERK paralleled with a reduction in p38 and JNK was also revealed by MAPK pathway studies, after administration of these drugs. Interestingly, the aforementioned changes induced by both drugs were reversed by administration of the specific PPAR-γ antagonist, GW9662. However, we found that azilsartan upregulated PPAR-γ to a lesser extent as compared to telmisartan and the latter may be preferred in hypertensive patients at risk of myocardial infarction.

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“…Paradoxically, the process of myocardial reperfusion also induces a series of adverse cardiac events such as inflammation, necrosis, apoptosis and autophagy, ultimately leading to myocardial ischaemia/reperfusion (I/R) injury [2]. Recent evidence has suggested that excessive inflammation and oxidative stress play predominant roles in the initiation and progression of I/R injury [3,4].…”

Section: Introductionmentioning

confidence: 99%

Overexpression of IκBα in cardiomyocytes alleviates hydrogen peroxide-induced apoptosis and autophagy by inhibiting NF-κB activation

et al. 2020

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Background: Inflammation and oxidative stress play predominant roles in the initiation and progression of ischaemia/reperfusion (I/R) injury, with nuclear factor kappa B (NF-κB) serving as a crucial mediator. Overexpression of the inhibitor of κB alpha (IκBα) gene is hypothesized to have protective effects against apoptosis and autophagy in cardiomyocytes subjected to hydrogen peroxide (H 2 O 2) by inhibiting the NF-κB pathway. Methods: The IκBα S32A, S36A gene was transfected via adeno-associated virus serotype 9 (AAV9) delivery into neonatal rat ventricular cardiomyocytes (NRVMs) prior to H 2 O 2 treatment. NRVMs were divided into control, H 2 O 2 , GFP + H 2 O 2 , IκBα+H 2 O 2 , and pyrrolidine dithiocarbamate (PDTC) + H 2 O 2 groups. Nuclear translocation of the NF-κB p65 subunit was evaluated by immunofluorescence and Western blotting. Cell viability was assessed by Cell Counting Kit-8 assay. Supernatant lactate dehydrogenase (LDH) and intracellular malondialdehyde (MDA) were measured to identify H 2 O 2-stimulated cytotoxicity. Apoptosis was determined by Annexin V-PE/7-AAD staining, and the mitochondrial membrane potential (ΔΨm) was detected by JC-1 staining. Western blotting was used to detect apoptosis-and autophagy-related proteins. Results: IκBα transfection significantly increased cell viability and ΔΨm but decreased the supernatant LDH and cellular MDA levels in cardiomyocytes exposed to H 2 O 2. Meanwhile, IκBα overexpression decreased H 2 O 2-induced apoptosis by upregulating the Bcl-2/Bax ratio and reduced autophagy by downregulating the expression of Beclin-1 and the LC3-II/LC3-I ratio. These effects partly accounted for the ability of IκBα to inhibit the NF-κB signalling pathway, as evidenced by decreases in p65 phosphorylation and nuclear translocation. Indeed, the effects of inactivation of NF-κB signalling with the specific inhibitor PDTC resembled the cardioprotective effects of IκBα during H 2 O 2 stimulation.

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Attenuation of ROS-mediated myocardial ischemia–reperfusion injury by morin via regulation of RISK/SAPK pathways

Cited by 16 publications

References 42 publications

Tiliacora triandra attenuates cisplatin triggered hepatorenal and testicular toxicity in rats by modulating oxidative inflammation, apoptosis and endocrine deficit

Tiliacora triandra attenuates cisplatin triggered hepatorenal and testicular toxicity in rats by modulating oxidative inflammation, apoptosis and endocrine deficit

Cardioprotective effects of azilsartan compared with that of telmisartan on an in vivo model of myocardial ischemia‐reperfusion injury

Overexpression of IκBα in cardiomyocytes alleviates hydrogen peroxide-induced apoptosis and autophagy by inhibiting NF-κB activation

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