Sepsis increases the risk of the liver injury development. According to the research works, coenzyme Q10 exhibits hepatoprotective properties in vivo as well as in vitro. Current work aimed at investigating the protective impacts of coenzyme Q10 against liver injury in septic BALB/c mice. The male BALB/c mice were randomly segregated into 4 groups: the control group, the coenzyme Q10 treatment group, the puncture and cecal ligation group, and the coenzyme Q10+cecal ligation and puncture group. Cecal ligation and puncture was conducted after gavagaging the mice with coenzyme Q10 during two weeks. Following 48 h postcecal ligation and puncture, we estimated hepatic biochemical parameters and histopathological changes in hepatic tissue. We evaluated the expression of factors associated with autophagy, pyroptosis, and inflammation. Findings indicated that coenzyme Q10 decreased the plasma levels in alkaline phosphatase, alanine aminotransferase, and aspartate aminotransferase in the cecal ligation and puncture group. Coenzyme Q10 significantly inhibited the elevation of sequestosome-1, interleukin-1, oligomerization domain-like receptor 3 and nucleotide-binding, interleukin-6, and tumor necrosis factor- expression levels; coenzyme Q10 also increased beclin 1 levels. Coenzyme Q10 might be a significant agent in the treatment of liver injury induced by sepsis.
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http://dx.doi.org/10.1155/2020/7598375 | DOI Listing |
FASEB J
January 2025
Department of General Surgery, Sir Run Run Hospital of Nanjing Medical University, Nanjing, Jiangsu, P. R. China.
NADH dehydrogenase (ubiquinone) 1 alpha subcomplex, 4-like 2 (NDUFA4L2) protein is located in the mitochondria and can regulate cell proliferation. Some studies have shown that the high NDUFA4L2 expression is linked with poor prognosis and cancer progression in various patients with cancers. However, the correlation between NDUFA4L2 and pan-cancer is unknown.
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January 2025
Museum of Natural History, University of Wroclaw, Wroclaw, Poland.
Background: Legless lizards, the slow worms of the genus are forming secondary contact zones within their Europe-wide distribution.
Methods: We examined 35 populations of and to identify the level of morphological and genetic divergence in Poland. We applied a conventional study approach using metric, meristic, and categorial (coloration) features for a phenotype analysis, and two standard molecular markers, a mitochondrial (NADH-ubiquinone oxidoreductase chain 2; ) and a nuclear (V(D)J recombination-activating protein 1; ) one.
J Hum Hypertens
January 2025
Geriatrics Center & National Clinical Research Center for Aging and Medicine, Jing'an District Central Hospital of Shanghai, Fudan University, Shanghai, China.
Previous studies suggest that ferroptosis is involved in cardiovascular diseases. The aim of the present study is to investigate the causal relationship between angiotensin II type 1 and type 2 receptors (ATR) activities and mitochondrial dysfunction in induction of cardiomyocyte ferroptosis. Human AC16 cardiomyocytes were first pre-treated with an ATR blockers, before stimulated with angiotensin II (Ang II) for 24 h.
View Article and Find Full Text PDFJ Neurochem
January 2025
The Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Bethesda, Maryland, USA.
Alzheimer disease is a neurodegenerative pathology-modifying mitochondrial metabolism with energy impairments where the effects of biological sex and DNA repair deficiencies are unclear. We investigated the therapeutic potential of dietary ketosis alone or with supplemental nicotinamide riboside (NR) on hippocampal intermediary metabolism and mitochondrial bioenergetics in older male and female wild-type (Wt) and 3xTgAD-DNA polymerase-β-deficient (3xTg/POLβ) (AD) mice. DNA polymerase-β is a key enzyme in DNA base excision repair (BER) of oxidative damage that may also contribute to mitochondrial DNA repair.
View Article and Find Full Text PDFFree Radic Biol Med
January 2025
Department of Neurology, Columbia University Medical Center, New York, NY, 10032, USA. Electronic address:
Coenzyme Q (CoQ) is a critical component of the mitochondrial respiratory chain. CoQ deficiencies often cause a variety of clinical syndromes, often involving encephalopathies. The heterogeneity of clinical manifestations implies different pathomechanisms, reflecting CoQ involvement in several biological processes.
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