Erdosteine salvages cardiac necrosis: Novel effect through modulation of MAPK and Nrf‐2/HO‐1 pathway

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

doi:10.1002/jbt.22590

Cited by 4 publications

(4 citation statements)

References 39 publications

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“…TUNEL assay was performed as given by Mutneja et al [ 27 ]. Heart sections were incubated with proteinase K for permeabilizing the apoptotic cells.…”

Section: Methodsmentioning

confidence: 99%

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Abatacept: A Promising Repurposed Solution for Myocardial Infarction-Induced Inflammation in Rat Models

Verma,

Mutneja,

Malik

et al. 2024

Oxidative Medicine and Cellular Longevity

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Myocardial infarction (MI) is irreversible damage to the myocardial tissue caused by prolonged ischemia/hypoxia, subsequently leading to loss of contractile function and myocardial damage. However, after a perilous period, ischemia-reperfusion (IR) itself causes the generation of oxygen free radicals, disturbance in cation homeostasis, depletion of cellular energy stores, and activation of innate and adaptive immune responses. The present study employed Abatacept (ABT), which is an anti-inflammatory drug, originally used as an antirheumatic response agent. To investigate the cardioprotective potential of ABT, primarily, the dose was optimized in a chemically induced model of myocardial necrosis. Thereafter, ABT optimized the dose of 5 mg/kg s.c. OD was investigated for its cardioprotective potential in a surgical model of myocardial IR injury, where animals (n = 30) were randomized into five groups: Sham, IR-C, Telmi10 + IR (Telmisartan, 10 mg/kg oral OD), ABT5 + IR, ABT perse. ABT and telmisartan were administered for 21 days. On the 21st day, animals were subjected to LAD coronary artery occlusion for 60 min, followed by reperfusion for 45 min. Further, the cardioprotective potential was assessed through hemodynamic parameters, oxidant–antioxidant biochemical enzymatic parameters, cardiac injury, inflammatory markers, histopathological analysis, TUNEL assay, and immunohistochemical evaluation, followed by immunoblotting to explore signaling pathways. The statistics were performed by one-way analysis of variance, followed by the Tukey comparison post hoc tests. Noteworthy, 21 days of ABT pretreatment amended the hemodynamic and ventricular functions in the rat models of MI. The cardioprotective potential of ABT is accompanied by inhibiting MAP kinase signaling and modulating Nrf-2/HO-1 proteins downstream signaling cascade. Overall, the present work bolsters the previously known anti-inflammatory role of ABT in MI and contributes a mechanistic insight and application of clinically approved drugs in averting the activation of inflammatory response.

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“…TUNEL assay was performed as given by Mutneja et al [ 27 ]. Heart sections were incubated with proteinase K for permeabilizing the apoptotic cells.…”

Section: Methodsmentioning

confidence: 99%

“…Terminal Deoxynucleotidyl Transferase dUTP Nick End Labeling (TUNEL) Assay. TUNEL assay was performed as given by Mutneja et al [27]. Heart sections were incubated with proteinase K for permeabilizing the apoptotic cells.…”

Section: Histopathological and Immunohistochemical Analysismentioning

confidence: 99%

Abatacept: A Promising Repurposed Solution for Myocardial Infarction-Induced Inflammation in Rat Models

Verma,

Mutneja,

Malik

et al. 2024

Oxidative Medicine and Cellular Longevity

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“…A large number of experimental studies have shown that inhibiting or blocking MAPK signaling pathway can reduce myocardial oxygen consumption, improve myocardial ischemia and injury, and inhibit myocardial fibrosis [8][9][10]. It also exhibits anti-inflammatory, anti-apoptotic and antioxidant activities to a certain extent [11]. Studying the expression of serum MAPK signaling pathway in patients with ventricular premature contractions is conducive to verifying the regulatory role of MAPK signaling pathway in the pathogenesis of ventricular premature contractions, and observing the related changes of MAPK and inflammatory factors is helpful to understand the regulatory role of this pathway in the inflammatory response of patients.…”

Section: Introductionmentioning

confidence: 99%

To Investigate the Pathogenesis and Inflammatory Response of Premature Ventricular Contractions Based on MAPK Signaling Pathway

2022

MEDSC

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Objective: To explore the involvement of MAPK signaling pathway in the pathogenesis of premature ventricular contractions (PVCs) and the regulation of inflammatory response. Methods: A total of 40 patients with PVCs admitted to Xi'an Hospital of Traditional Chinese Medicine from June 2021 to December 2021 were randomly selected as the observation group, and 40 healthy subjects during the same period were selected as the control group. Blood samples were collected intravenously, and the levels of MAPK, IL-1β, IL-6 and TNF-αin serum of the subjects were detected by enzyma-linked immunosorbent assay (ELISA). To analyze the relationship between MAPK signaling pathway and PVC and regulation of inflammatory response. Results: Compared with the control group, the levels of serum MAPK and inflammatory factors IL-1β, IL-6 and TNFαin observation group were significantly increased (P<0.05), and the expression of MAPK signaling pathway was highly positively correlated with the levels of inflammatory factors IL-1β, IL-6 and TNF-αin observation group. Conclusion: The pathogenesis of PVCs may be related to MAPK signaling pathway and inflammatory response. PVCs may promote the release of IL-1β, IL-6 and TNF-α by activating MAPK signaling pathway, up-regulating MAPK expression, and inducing inflammatory response.

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“…Its broad-spectrum dose (LD50: 3500–5000 mg/kg) has protective effects on many diseases [ 23 ]. Mutneja et al showed that erdosteine attenuated myocardial necrosis induced by isoproterenol (ISO) by inhibiting the MAPK and Nrf-2/HO-1 pathways [ 24 ]. In another study, Ugurel et al reported that erdosteine can protect the ovaries from torsional/resetting damage by avoiding scavenging free radicals, releasing oxidative free radicals, and by blocking pro-inflammatory processes [ 25 ].…”

Section: Introductionmentioning

confidence: 99%

Tissue-Protective Effect of Erdosteine on Multiple-Organ Injuries Induced by Fine Particulate Matter

et al. 2021

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Background Fine particulate matter (PM2.5) is the air pollutant that most threatens global public health. The purpose of this study was to observe the inflammatory and oxidative stress injury of multiple organs induced by PM2.5 in rats and to explore the tissue-protective effect of erdosteine. Material/Methods We randomly divided 40 male Wistar rats into a blank control group, a saline group, a PM2.5 exposure group, and an erdosteine intervention group. We assessed changes in organs tissue homogenate and biomarkers of inflammation and oxidative stress in serum and bronchoalveolar lavage fluid (BALF). Results (1) The expressions of IL-6, IL-1β, TNF-α, 8-OHdG, 4-HNE, and PCC in serum and BALF of the PM2.5 exposure group increased, but decreased after treatment with erdosteine, suggesting that erdosteine treatment attenuates inflammatory and oxidative stress injury. (2) The expression of γ-GCS in serum and lungs in the PM2.5 exposure group increased, but did not change significantly after treatment with erdosteine. This suggests that PM2.5 upregulates the level of γ-GCS, while erdosteine does not affect this protective response. (3) The expression of T-AOC in serum, lungs, spleens, and kidneys of the PM2.5 exposure group decreased, but increased after treatment with erdosteine. Our results suggest that PM2.5 can cause imbalance of oxidation/anti-oxidation in multiple organs, and erdosteine can alleviate this imbalance. Conclusions PM2.5 exposure can lead to inflammatory and oxidative stress damage in serum and organ tissues of rats. Erdosteine may be an effective anti-inflammatory and antioxidant that can reduce this injury.

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Erdosteine salvages cardiac necrosis: Novel effect through modulation of MAPK and Nrf‐2/HO‐1 pathway

Cited by 4 publications

References 39 publications

Abatacept: A Promising Repurposed Solution for Myocardial Infarction-Induced Inflammation in Rat Models

Abatacept: A Promising Repurposed Solution for Myocardial Infarction-Induced Inflammation in Rat Models

To Investigate the Pathogenesis and Inflammatory Response of Premature Ventricular Contractions Based on MAPK Signaling Pathway

Tissue-Protective Effect of Erdosteine on Multiple-Organ Injuries Induced by Fine Particulate Matter

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