Role of MAPK/NF-κB pathway in cardioprotective effect of Morin in isoproterenol induced myocardial injury in rats

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

doi:10.1007/s11033-018-04575-9

Cited by 58 publications

(35 citation statements)

References 46 publications

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“…While ERK which promotes cell survival was diminished within myocardium. Inhibiting MAPK pathway had revealed to protect against myocardial injury in the experimental animals as mentioned previously [21,22,29]. Triggering JNK was presented to have a pro-apoptotic role in ISO induced apoptosis [30].…”

Section: A B Cmentioning

confidence: 73%

“…Isoproterenol (ISO), β adrenergic agonist, in high doses, can upsurges myocardial burden, triggering myocardial dysfunction in animals mimicking the pathological and morphological deviations happening in humans. Augmented free radicals production during MI causes stimulation of mitogen activated protein kinase (MAPK) signaling pathway [21].…”

Section: Introductionmentioning

confidence: 99%

“…MAPK involve three subfamilies; Extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun-N-terminal kinase (JNK) and p38. MAPK signaling pathway promote NF-κB, which provokes additional inflammatory cytokines triggering extra injury within the myocardium tissue [21]. ERK signaling pathway, the most studied, is involved in regulating multiple biological processes, such as survival, growth and death of various cells and inflammationrelated immune response [22].…”

Section: Introductionmentioning

confidence: 99%

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D-Limonene mitigate myocardial injury in rats through MAPK/ERK/NF-κB pathway inhibition

Younis

2020

Korean J Physiol Pharmacol

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Cardiovascular diseases are the primary reason of mortality, among which myocardial infarction (MI) is the most dominant and prevalent. This study was considered to examine D-Limonene protective action against isoproterenol (ISO) induced MI. Wister male rats were dispersed into four groups. Normal and D-Limonene control group in which rats administered saline or D-Limonene. ISO control animals were administered saline for 21 days then challenged with ISO (85 mg/kg, subcutaneously) on 20th and 21st day for MI induction. D-Limonene pretreated group in which animals were pretreated with D-Limonene 50 mg/kg orally for 21 days then administered ISO on 20th and 21st day. MI prompted variations were assessed by myocardial infarction area determination, blood pressure (BP) alterations, cardiac injury biomarkers and inflammatory mediators measurements. For more depth investigation, both the apoptotic status was evaluated via measuring mRNA expression of Bcl-2 and Bax as well as mitogen-activated protein kinase-extracellular signal-regulated kinase (MAPK-ERK) signal transduction were investigated via Western blotting. MI group revealed significant infarcted area, blood pressure alterations, myocardial injury enzymes intensification together with inflammatory cytokines amplification. MI was associated with activation of MAPK-ERK signal pathway and apoptotic status within the myocardium. On the other hand, pretreated with D-Limonene demonstrated deterred infracted area, reduced myocardial enzymes, improved BP indices, lessened inflammatory levels. Furthermore, D-Limonene pretreatment caused a decline in MAPK proteins pathway and Bax relative mRNA expression, while intensifying Bcl-2 mRNA expression promoting that D-Limonene may constrain MI induced myocardial apoptosis. D-Limonene mitigated MI injury through MAPK/NF-κB pathway inhibition and anti-apoptotic effect.

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Section: A B Cmentioning

confidence: 73%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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D-Limonene mitigate myocardial injury in rats through MAPK/ERK/NF-κB pathway inhibition

Younis

2020

Korean J Physiol Pharmacol

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“…MI is triggered by deficient myocardial oxygen supply as compared to demand, resulting in myocardial hypoxia and subsequent buildup of metabolites as waste. This is followed by several biochemical changes, such as free radical destruction, upsurge in cardiac indicators, and pro-inflammatory cytokines [35], oxidative stress, calcium overload, myocardial and endothelial injury, contractile dysfunction, necrosis, and /or apoptosis induced cell death [36]. Oxidative stress is one of the major mechanisms elaborated in myocardial infarction and cardiotoxicity pathogenesis.…”

Section: Discussionmentioning

confidence: 99%

Cyanobacteria as Nanogold Factories II: Chemical Reactivity and anti-Myocardial Infraction Properties of Customized Gold Nanoparticles Biosynthesized by Cyanothece sp.

et al. 2019

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Cyanothece sp., a coccoid, unicellular, nitrogen-fixing and hydrogen-producing cyanobacterium, has been used in this study to biosynthesize customized gold nanoparticles under certain chemical conditions. The produced gold nanoparticles had a characteristic absorption band at 525–535 nm. Two types of gold nanoparticle, the purple and blue, were formed according to the chemical environment in which the cyanobacterium was grown. Dynamic light scattering was implemented to estimate the size of the purple and blue nanoparticles, which ranged from 80 ± 30 nm and 129 ± 40 nm in diameter, respectively. The highest scattering of laser light was recorded for the blue gold nanoparticles, which was possibly due to their larger size and higher concentration. The appearance of anodic and cathodic peaks in cyclic voltammetric scans of the blue gold nanoparticles reflected the oxidation into gold oxide, followed by the subsequent reduction into the nano metal state. The two produced forms of gold nanoparticles were used to treat isoproterenol-induced myocardial infarction in experimental rats. Both forms of nanoparticles ameliorated myocardial infarction injury, with a slight difference in their curative activity with the purple being more effective. Mechanisms that might explain the curative effect of these nanoparticles on the myocardial infarction were proposed. The morphological, physiological, and biochemical attributes of the Cyanothece sp. cyanobacterium were fundamental for the successful production of “tailored” nanoparticles, and complemented the chemical conditions for the differential biosynthesis process. The present research represents a novel approach to manipulate cyanobacterial cells towards the production of different-sized gold nanoparticles whose curative impacts vary accordingly. This is the first report on that type of manipulated gold nanoparticles biosynthesis which will hopefully open doors for further investigations and biotechnological applications.

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“…P38 causes inflammation and apoptosis, which are the key markers of ISO-induced myocardial necrosis. [10] Moreover, these proteins are also associated with several other pathways, which can cause cellular damage and are still unexplored.…”

Section: Introductionmentioning

confidence: 99%

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

Mutneja

Verma

Malik

et al. 2020

J Biochem & Molecular Tox

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Isoproterenol (ISO) induced oxidative stress and inflammation is involved in the pathogenesis of myocardial necrosis. To optimize the effect of erdosteine against myocardial necrosis, male albino Wistar rats were divided into eight groups (n = 6), that is, normal, ISO-control, erdosteine pretreatment with ISO. Rats were administered erdosteine orally for 28 days. Two doses of ISO (85 mg/kg), s.c. were given to ISO-C and erdosteine treatment groups on the 27th and 28th day. On the 29th day, hemodynamic parameters were recorded and the heart was excised for further parameters. In ISO-C rats, significantly increased levels of inflammatory markers, pro-oxidants, and structural damage were observed as compared with normal group. Furthermore, immunohistochemistry and terminal deoxynucleotidyl transferase dUTP nick end labeling revealed an increased expression of apoptotic proteins. Erdosteine at 80 mg/kg reversed the deleterious effects of ISO and normalized myocardium. Erdosteine showed anti-inflammatory, antiapoptotic, and antioxidant activities through inhibition of MAPK and Nrf-2/HO-1 pathways. To conclude, erdosteine was found protective in ISOinduced myocardial necrosis through MAPK and Nrf-2/HO-1 pathway.

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Role of MAPK/NF-κB pathway in cardioprotective effect of Morin in isoproterenol induced myocardial injury in rats

Cited by 58 publications

References 46 publications

D-Limonene mitigate myocardial injury in rats through MAPK/ERK/NF-κB pathway inhibition

D-Limonene mitigate myocardial injury in rats through MAPK/ERK/NF-κB pathway inhibition

Cyanobacteria as Nanogold Factories II: Chemical Reactivity and anti-Myocardial Infraction Properties of Customized Gold Nanoparticles Biosynthesized by Cyanothece sp.

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

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