Coenzyme Q10 prevents oxidative stress and fibrosis in isoprenaline induced cardiac remodeling in aged rats

Ulla, Anayt; Mohamed, Mustafe; Sikder, Biswajit; Rahman, Afm Towheedur; Sumi, Farzana Akther; Hossain, Murad; Reza, Hasan Mahmud; Rahman, Ghazi Muhammad Sayedur; Alam, Muhammad Ashraful

doi:10.1186/s40360-017-0136-7

Cited by 61 publications

(43 citation statements)

References 61 publications

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“…It has become more apparent that oxidative stress in cardiac cells could lead to adverse cardiac remodeling including cell death and myocardial hypertrophy . During MIRI, oxidative stress (induced by excessive ROS) emerges as a cause of endothelial dysfunction in the heart .…”

Section: Discussionmentioning

confidence: 99%

“…It has become more apparent that oxidative stress in cardiac cells could lead to adverse cardiac remodeling including cell death and myocardial hypertrophy. 23 During MIRI, oxidative stress (induced by excessive ROS) emerges as a cause of endothelial dysfunction in the heart. 24 Excessive ROS can initiate lipid peroxidation, cause DNA damage, and induce several biological effects, including pro-apoptosis, proinflammation, and anti-proliferation by stimulating various signal pathway.…”

Section: Discussionmentioning

confidence: 99%

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miR‐200a mediates protection of thymosin β‐4 in cardiac microvascular endothelial cells as a novel mechanism under hypoxia‐reoxygenation injury

Zhu

Liu

et al. 2019

J of Cellular Biochemistry

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Thymosin β‐4 (Tβ4) is a ubiquitous protein, which has been suggested to regulate multiple cell signal pathways and a variety of cellular functions. However, the role Tβ4 plays in the cardiac microvascular endothelial cells (CMECs) under myocardial ischemia/reperfusion injury is currently unknown. Here we investigated the effects of Tβ4 on hypoxia/reoxygenation (H/R) induced CMECs injury and its potential molecular mechanism. Cultured CMECs were positively identified by flow cytometry using antibody against CD31 and VWF/Factor VIII, which are constitutively expressed on the surface of CMECs. Then the reduced level of Tβ4 was detected in H/R‐CMECs by a real‐time quantitative polymerase chain reaction. To determine the effects of Tβ4 on H/R‐CMECs, we transfected the overexpression or silence vector of Tβ4 into CMECs under H/R condition. Our results indicated that H/R treatment could reduce proliferation, increased apoptosis, adhesion, and reactive oxygen species (ROS) production in CMECs, which were attenuated by Tβ4 overexpression or aggravated by Tβ4 silencing, implying Tβ4 is able to promote CMECs against H/R‐induced cell injury. Furthermore, the microRNA‐200a (miR‐200a) level was also increased by Tβ4 in H/R‐CMECs or reduced by Tβ4 small interfering RNA. To investigated the mechanism of protective effects of Tβ4 on CMECs injury, the miR‐200a inhibitor was transfected into H/R‐CMECs. The results indicated that inhibition of miR‐200a inversed the protection of Tβ4 on H/R‐CMECs, specifically including cell proliferation, cell adhesion, cell apoptosis, and ROS production, as well as nuclear factor erythroid 2‐related factor 2 (Nrf2) nuclear translocation. In conclusion, our results determined that Tβ4 attenuated H/R‐induced CMECs injury by miR‐200a‐Nrf2 signaling.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

miR‐200a mediates protection of thymosin β‐4 in cardiac microvascular endothelial cells as a novel mechanism under hypoxia‐reoxygenation injury

Zhu

Liu

et al. 2019

J of Cellular Biochemistry

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“…Відповідно до мітохондріальної теорії старіння, основний фактор у розвитку вікових змін в органах і тканинах цілісного організмузміни функціонального стану мітохондрій, що викликає надмірне утворення активних форм оксигену (Judge and Leeuwenburgh, 2007;Marques et al, 2015;Anayt et al, 2017).…”

Section: вступunclassified

“…Низка дослідників показали, що існує пряма залежність між умістом і активністю антиоксидантних ензимів у організмі та тривалістю життя (Anayt et al, 2017;Lykhatskyi and Fira, 2017). Пропонується гіпотеза, що, можливо, старіння пов'язане зі зниженням ензиматичної активності антиоксидантів.…”

Section: вступunclassified

“…З огляду на це, встановлений рівень ТБК-активних продуктів означає, що процеси ПОЛ і руйнування протеїнів клітинних мембран уже відбулися, і система антиоксидантного захисту намагається пристосуватися до таких навантажень для забезпечення енантіостазу. Це підтверджується літературними даними (Judge and Leeuwenburgh, 2007;Marques et al, 2015;Anayt et al, 2017).…”

Section: обговоренняunclassified

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The role of mitochondria in the myocardium of senescent Meriones unguiculates

Potapenko¹,

Dyomshina²,

Ушакова³

2017

Regul. Mech. Biosyst.

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According to the mitochondrial theory of aging, changes in the functional state of mitochondria, which lead to excessive formation of active forms of oxygen, are the main factor in the development of age changes in organs and tissues of the whole organism. The assessment of the mitochondria state of the heart of senescent gerbils (Mongolian Gerbilia, Meriones unguiculates Milne-Edwards, 1867). It is proved that the aging of the heart is preceded by the appearance of dysfunction in mitochondria. The disturbance of metabolic processes in the myocardium of gerbils over the age of two years was established, which was accompanied by activation of oxidative stress by increasing the concentration of TBK-active compounds. An increase in the concentration of cytochrome C in cytosol has been shown due to the destructive effects of oxidized products on the outer membrane of mitochondria and enhancement of its permeability. The violation of bioenergetic processes, increase of the anaerobic respiration and the accumulation of lactate and unoxidative metabolites, which increases oxidative stress and cell damage, are determined. We established that for gerbils the critical age for senescence is 24 months. Major metabolic changes in the heart occur mostly at this age. This is marked by activation of prooxidants formation, proteolytic processes (decrease in total protein concentration) and inhibition of aminotransferase activity in cytosol. The switching of metabolic processes in the mitochondria of the heart with the participation of aminotransferases has been registered: increased activity of the mitochondrial isoenzyme alanine aminotransferase and reciprocal reduction of aspartate aminotransferase. After two years of age in the experimental gerbils the intensification of adaptive processes was established: activation of catalase, γ-glutamyltransferase, relative restoration of the activity of alanine and aspartate aminotransferase, thus maintaining the processes of the vital activity of the whole organism, but at a new metabolic level. With age, irreversible damage to cardiomyocytes occurs, which gradually lose the ability to convert lactate, resulting in its increase, and the processes of its utilization are inhibited. The results confirm the key role of mitochondria in the process of aging of the myocardium. However, when gerbils reach the 36 months of age the metabolic disturbances in the myocardium reach their peak, resulting in large-scale cell damage. Роль мітохондрій міокарда піщанок упродовж фізіологічного старінняЄ. О. Потапенко, О. О. Дьомшина, Г. О. Ушакова Дніпровський національний університет імені Олеся Гончара, Дніпро, УкраїнаНаведено дані щодо оцінки мітохондрій та біохімічного стану серця монгольських піщанок (Mongolian Gerbilia, Meriones unguiculatus Milne-Edwards, 1867) в умовах старіння. Основний фактор розвитку вікових змін в органах і тканинах цілісного організмунадмірне утворення активних форм оксигену, що провокує зміни функціонального стану мітохондрій, зниження ефективності процесу аутофагії / мітофаг...

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Possible protective effects of CO Q10 against vincristine‐induced peripheral neuropathy: Targeting oxidative stress, inflammation, and sarmoptosis

Elshamy

Salem

Safa

et al. 2021

J Biochem & Molecular Tox

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Vincristine is a chemotherapy drug that belongs to the vinca alkaloids group. It is used for treatment of hematologic malignancies and several solid tumors.Vincristine-induced peripheral neuropathy is a major dose-limiting side effect.Coenzyme Q10 (Co Q10), an essential component of the mitochondrial electron transport chain, participates in energy production. It is a powerful fat-soluble antioxidant and also exerts anti-inflammatory effects. Therefore, this study was aimed to focus on the mechanistic insights of vincristine-induced peripheral neuropathy in addition to shedding the light on the modulatory effect of Co Q10.Twenty-eight rats were randomly divided into four groups. Peripheral neuropathy was induced by intraperitoneal injection of vincristine (0.1 mg/kg body weight).Co Q10 was injected intraperitoneally (10 mg/kg body weight) for 24 days. Sciatic nerve MDA, TAC, GSH, 8-OHdG, TNF-α, IL-1β, and NF-κB levels were assessed. Gene expression of SARM1 andNrf2 was also assessed. Serum neurofilament light chain was immunoassayed, in addition to the behavioral assessment. Co Q10 significantly improved oxidative stress and inflammatory biomarkers. It also decreased serum NFL levels. It enhanced Nrf2 and decreased SARM1 gene expression. Histopathological findings proved the biochemical and molecular findings. Our results support Co Q10 as a potential protective agent against vincristine-induced peripheral neuropathy.

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Coenzyme Q10 prevents oxidative stress and fibrosis in isoprenaline induced cardiac remodeling in aged rats

Cited by 61 publications

References 61 publications

miR‐200a mediates protection of thymosin β‐4 in cardiac microvascular endothelial cells as a novel mechanism under hypoxia‐reoxygenation injury

miR‐200a mediates protection of thymosin β‐4 in cardiac microvascular endothelial cells as a novel mechanism under hypoxia‐reoxygenation injury

The role of mitochondria in the myocardium of senescent Meriones unguiculates

Possible protective effects of CO Q10 against vincristine‐induced peripheral neuropathy: Targeting oxidative stress, inflammation, and sarmoptosis

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