Attenuation of oxidative stress-induced lesions in skeletal muscle in a mouse model of obesity-independent hyperlipidaemia and atherosclerosis through the inhibition of Nox2 activity

Sfyri, Pagona Panagiota; Yuldasheva, Nadira; Tzimou, Anastasia; Giallourou, Natasa; Crispi, Vassili; Aburima, Ahmed; Beltrán-Álvarez, Pedro; Patel, Ketan; Mougios, Vassilis; Swann, Jonathan R.; Kearney, Mark T.; Matsakas, Antonios

doi:10.1016/j.freeradbiomed.2018.10.422

Cited by 15 publications

(24 citation statements)

References 90 publications

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“…One study has confirmed that TMZ enhanced mitochondrial respiratory function and promoted mitochondrial biosynthesis in cardiomyocytes (Shi, Shangguan, Zhang, Li, & Li, ). A recent study also showed that TMZ attenuated SMV‐associated skeletal muscle injury in ApoE −/− mice (Song et al, ), which is an established model of atherosclerosis that develops hyperlipidaemia and atherosclerotic (Sfyri et al, ).…”

Section: Introductionmentioning

confidence: 97%

Astragaloside IV reverses simvastatin‐induced skeletal muscle injury by activating the AMPK‐PGC‐1α signalling pathway

Jiang

Yang

Dang

et al. 2019

Phytotherapy Research

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In this study, we investigated the effect of astragaloside IV on skeletal muscle energy metabolism disorder caused by statins and explored the possible mechanisms. Highfat diet-fed apolipoprotein E knockout (ApoE −/− ) mice performed aerobic exercise and were administered simvastatin, simvastatin + trimetazidine, or simvastatin + astragaloside IV by gavage. At the end of treatment, exercise performance was assessed by the hanging grid test, forelimb grip test, and running tolerance test.Moreover, plasma lipid and creatine kinase concentrations were measured. After sacrifice, the gastrocnemius muscle was used to assess muscle morphology, and energy metabolism was evaluated by determining the concentration of lactic acid and the storage capacity of adenosine triphosphate and glycogen. Mitochondrial function was assessed by measuring mitochondrial complex III and citrate synthase activity and membrane potential. In addition, oxidative stress was assessed by determining the level of hydrogen peroxide. Finally, using western blotting and reverse transcription polymerase chain reaction, we explored the mechanism of astragaloside IV in alleviating simvastatin-induced muscle injury. Our results demonstrated that astragaloside IV reversed simvastatin-induced muscle injury without affecting the lipid-lowering effect of simvastatin. Moreover, astragaloside IV promoted the phosphorylation of AMPK and activated PGC-1α, which upregulated the expression of NRF1 to enhance energy metabolism and inhibit skeletal muscle cell apoptosis. K E Y W O R D Sastragaloside IV, energy metabolism, mitochondria, simvastatin, skeletal muscle injury

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Section: Introductionmentioning

confidence: 97%

Astragaloside IV reverses simvastatin‐induced skeletal muscle injury by activating the AMPK‐PGC‐1α signalling pathway

Jiang

Yang

Dang

et al. 2019

Phytotherapy Research

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“…Recent evidence indicates a direct link between the production of diet‐induced reactive oxygen species (ROS) and levels of oxidative protein modifications such as 4‐hydroxynonenal (4‐HNE) and 3‐nitrotyrosine (3NT) adducts that are involved in the development of metabolic disorders . Loss of CD36 is known to attenuate ROS production, alleviating oxidative stress .…”

Section: Resultsmentioning

confidence: 99%

“…Gastrocnemius and liver lipid profiling was performed by using a combination of thin‐layer chromatography and gas chromatography as previously described . Tissue was pulverized by manual mortar and pestle grinding in liquid nitrogen.…”

Section: Methodsmentioning

confidence: 99%

“…Recent evidence indicates a direct link between the production of diet-induced reactive oxygen species (ROS) and levels of oxidative protein modifications such as 4-hydroxynonenal (4-HNE) and 3-nitrotyrosine (3NT) adducts that are involved in the development of metabolic disorders. [29][30][31][32] Loss of CD36 is known to attenuate ROS production, alleviating oxidative stress. 33,34 Therefore, we sought to determine the impact of CD36 deficiency and HF diet on the redox homeostasis of the skeletal muscle, by measuring lipid peroxidation (thiobarbituric acid reactive substance; TBARS), protein oxidative modifications (3NT, 4-HNE), DNA damage (by means of Ogg1 relative mRNA expression) and ROS production (Dihydroethidium; DHE staining).…”

Section: Skeletal Muscle From Cd36 Ko Mice Is Protected From High-fmentioning

confidence: 99%

“…Gastrocnemius and liver lipid profiling was performed by using a combination of thin-layer chromatography and gas chromatography as previously described. 32,90 Tissue was pulverized by manual mortar and pestle grinding in liquid nitrogen. Lipids were extracted from specimens with chloroform-methanol 2:1 (v/v) in the presence of 0.005% (w/v) butylated hydroxytoluene, as an antioxidant, and fixed amounts of triheptadecanoyl glycerol (Sigma), as triacylglycerol internal standard, and diheptadecanoyl phosphatidyl choline (Larodan), as phospholipid internal standard.…”

Section: Gas Chromatographymentioning

confidence: 99%

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Loss of CD36 protects against diet‐induced obesity but results in impaired muscle stem cell function, delayed muscle regeneration and hepatic steatosis

et al. 2019

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Aim The prevalence of obesity is a major risk factor for cardiovascular and metabolic diseases including impaired skeletal muscle regeneration. Since skeletal muscle regenerative capacity is regulated by satellite cells, we aimed to investigate whether a high‐fat diet impairs satellite cell function and whether this is linked to fatty acid uptake via CD36. We also aimed to determine whether loss of CD36 impacts on muscle redox homeostasis and skeletal muscle regenerative capacity. Methods We studied the impact of a high‐fat diet and CD36 deficiency on murine skeletal muscle morphology, redox homeostasis, satellite cell function, bioenergetics and lipid accumulation in the liver. We also determined the effect of CD36 deficiency on skeletal muscle regeneration. Results High‐fat diet increased body weight, intramuscular lipid accumulation and oxidative stress in wild‐type mice that were significantly mitigated in CD36‐deficient mice. High‐fat diet and CD36 deficiency independently attenuated satellite cell function on single fibres and myogenic capacity on primary satellite cells. CD36 deficiency resulted in delayed skeletal muscle regeneration following acute injury with cardiotoxin. CD36‐deficient and wild‐type primary satellite cells had distinct bioenergetic profiles in response to palmitate. High‐fat diet induced hepatic steatosis in both genotypes that was more pronounced in the CD36‐deficient mice. Conclusion This study demonstrates that CD36 deficiency protects against diet‐induced obesity, intramuscular lipid deposition and oxidative stress but results in impaired muscle satellite cell function, delayed muscle regeneration and hepatic steatosis. CD36 is a key mediator of fatty acid uptake in skeletal muscle, linking obesity with satellite cell function and muscle regeneration.

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Effects of Apigenin on the Expression of LOX‐1, Bcl‐2, and Bax in Hyperlipidemia Rats

et al. 2021

Chemistry & Biodiversity

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We aimed to investigate the impact of apigenin on LOX‐1, Bcl‐2, and Bax expression in hyperlipidemia rats and explore the possible molecular pathological mechanism of apigenin in improving hyperlipidemia and preventing atherosclerosis. In hyperlipidemia models, the levels of total cholesterol (TC), triglyceride (TG), low‐density lipoprotein cholesterol (LDL‐c) and the LOX‐1 protein expression were apparently increased (P<0.01), while the high‐density lipoprotein cholesterol (HDL‐c) levels and the ratio of Bcl‐2/Bax were reduced significantly (P<0.01) in comparison with the standard control group. After the treatment of apigenin, the levels of TC, TG, LDL‐c, and the LOX‐1 protein expression were noticeably decreased (P<0.01), while the levels of HDL‐c and the Bcl‐2/Bax ratio were increased (P<0.01). The intima was thickened and had protrusions in the hyperlipidemia model group compared to the normal control group. In comparison with the atherosclerosis model group, the degree of aortic lesions in the low‐dose, middle‐dose, high‐dose groups was alleviated. Apigenin can reduce the level of blood lipid, improve hyperlipidemia, and prevent atherosclerosis in hyperlipidemia rats. The molecular mechanism may be related to inhibiting LOX‐1 gene expression and increasing the Bcl‐2/Bax ratio.

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Attenuation of oxidative stress-induced lesions in skeletal muscle in a mouse model of obesity-independent hyperlipidaemia and atherosclerosis through the inhibition of Nox2 activity

Abstract: Attenuation of oxidative stress-induced lesions in skeletal muscle in a mouse model of obesity-independent hyperlipidaemia and atherosclerosis through the inhibition of Nox2 activity, Free Radical Biology and Medicine,

Cited by 15 publications

References 90 publications

Astragaloside IV reverses simvastatin‐induced skeletal muscle injury by activating the AMPK‐PGC‐1α signalling pathway

Astragaloside IV reverses simvastatin‐induced skeletal muscle injury by activating the AMPK‐PGC‐1α signalling pathway

Loss of CD36 protects against diet‐induced obesity but results in impaired muscle stem cell function, delayed muscle regeneration and hepatic steatosis

Effects of Apigenin on the Expression of LOX‐1, Bcl‐2, and Bax in Hyperlipidemia Rats

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