1022 Mitochondria-Targeting Antioxidant Attenuates Carbon Tetracholride-Induced Liver Fibrosis

Rehman, Hasibur; Liu, Qinlong; Haque, Khujista; Krishnasamy, Yasodha; Ramshesh, Venkat K.; Lemasters, John J.; Murphy, Michael P.; Zhong, Zhi

doi:10.1016/s0016-5085(12)63650-6

Cited by 9 publications

(13 citation statements)

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“…Studies have demonstrated that SAC improved liver disease via regulation of the peroxisomal proliferator activator receptor α (PPAR-α), sterol regulatory element binding protein 1c (SREBP-1c), serum adiponectin levels, liver MDA, reactive oxygen species (ROS) content, serum ALT, serum AST, GSH content, GSH-Px and CAT activities, and the inhibition of lipolysis. Additionally, SAC can significantly inhibit N-nitrosodiethylamine (NDEA)-induced hepatocarcinogenesis [4,36,37,38]. We further analyzed the SAC content of EA, BA, and WS where, from the data, it was found that SAC only appeared in BA (497.58 ± 43.78 μg/g, Table 1).…”

Section: Discussionmentioning

confidence: 99%

Extracts from Fermented Black Garlic Exhibit a Hepatoprotective Effect on Acute Hepatic Injury

Tsai

Chen

et al. 2019

Molecules

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The mechanism of hepatoprotective compounds is usually related to its antioxidant or anti-inflammatory effects. Black garlic is produced from garlic by heat treatment and its anti-inflammatory activity has been previously reported. Therefore, the aim of this study was to investigate the hepatoprotective effect of five different extracts of black garlic against carbon tetrachloride (CCl4)-induced acute hepatic injury (AHI). In this study, mice in the control, CCl4, silymarin, and black garlic groups were orally administered distilled water, silymarin, and different fraction extracts of black garlic, respectively, after CCl4 was injected intraperitoneally to induce AHI. The results revealed that the n-butanol layer extract (BA) and water layer extract (WS) demonstrated a hepatoprotective effect by reducing the levels of alanine aminotransferase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), and hepatic malondialdehyde (MDA). Furthermore, the BA and WS fractions of black garlic extract increased the activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), glutathione reductase (GSH-Rd), tumor necrosis factor alpha (TNF-α), and the interleukin-1 (IL-1β) level in liver. It was concluded that black garlic exhibited significant protective effects on CCl4-induced acute hepatic injury.

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Section: Discussionmentioning

confidence: 99%

Extracts from Fermented Black Garlic Exhibit a Hepatoprotective Effect on Acute Hepatic Injury

Tsai

Chen

et al. 2019

Molecules

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“…Mitoquinone (MitoQ)—a mitochondria‐targeted anti‐oxidant—consists of co‐enzyme Q10 and a TPP cation that can easily accumulate several 100‐fold within the mitochondria, thereby making it more powerful than untargeted anti‐oxidants in preventing mitochondrial oxidative damage . In vitro and in vivo studies have demonstrated that MitoQ is protective against many oxidative damage‐related diseases . In addition, daily oral doses of 40 or 80 mg MitoQ have been shown to protect against liver damage in hepatitis C patients and can be safely administered to Parkinson's disease patients for up to 1 year .…”

Section: Introductionmentioning

confidence: 99%

“…25 In vitro and in vivo studies have demonstrated that MitoQ is protective against many oxidative damage-related diseases. [26][27][28][29][30][31][32][33] In addition, daily oral doses of 40 or 80 mg MitoQ have been shown to protect against liver damage in hepatitis C patients 34 and can be safely administered to Parkinson's disease patients for up to 1 year. 35 There is evidence that the protective effect of MitoQ is partially mediated by the modulation of mitochondrial dynamics, mitophagy and Nrf2 signalling.…”

Section: Introductionmentioning

confidence: 99%

The mitochondria‐targeted anti‐oxidant MitoQ protects against intervertebral disc degeneration by ameliorating mitochondrial dysfunction and redox imbalance

et al. 2020

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Objective Mitochondrial dysfunction, oxidative stress and nucleus pulposus (NP) cell apoptosis are important contributors to the development and pathogenesis of intervertebral disc degeneration (IDD). Here, we comprehensively evaluated the effects of mitochondrial dynamics, mitophagic flux and Nrf2 signalling on the mitochondrial quality control, ROS production and NP cell survival in in vitro and ex vivo compression models of IDD and explored the effects of the mitochondria‐targeted anti‐oxidant MitoQ and its mechanism. Material and methods Human NP cells were exposed to mechanical compression to mimic pathological conditions. Results Compression promoted oxidative stress, mitochondrial dysfunction and NP cell apoptosis. Mechanistically, compression disrupted the mitochondrial fission/fusion balance, inducing fatal fission. Concomitantly, PINK1/Parkin‐mediated mitophagy was activated, whereas mitophagic flux was blocked. Nrf2 anti‐oxidant pathway was insufficiently activated. These caused the damaged mitochondria accumulation and persistent oxidative damage. Moreover, MitoQ restored the mitochondrial dynamics balance, alleviated the impairment of mitophagosome‐lysosome fusion and lysosomal function and enhanced the Nrf2 activity. Consequently, damaged mitochondria were eliminated, redox balance was improved, and cell survival increased. Additionally, MitoQ alleviated IDD in an ex vivo rat compression model. Conclusions These findings suggest that comodulation of mitochondrial dynamics, mitophagic flux and Nrf2 signalling alleviates sustained mitochondrial dysfunction and oxidative stress and represents a promising therapeutic strategy for IDD; furthermore, our results provide evidence that MitoQ might serve as an effective therapeutic agent for this disorder.

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“…155 In mice experiments, mitoQ showed inhibition of HSCs activation and transforming growth factor-beta 1 expression, both key factors in hepatic fibrosis. 156,157 Targeting Farnesoid X Receptor…”

Section: Mitoqmentioning

confidence: 99%

Mitochondrial Dysfunction and Oxidative Stress in Liver Transplantation and Underlying Diseases: New Insights and Therapeutics

et al. 2021

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Mitochondria are essential organelles for cellular energy and metabolism. Like with any organ, the liver highly depends on the function of these cellular powerhouses. Hepatotoxic insults often lead to an impairment of mitochondrial activity and an increase in oxidative stress, thereby compromising the metabolic and synthetic functions. Mitochondria play a critical role in ATP synthesis and the production or scavenging of free radicals. Mitochondria orchestrate many cellular signaling pathways involved in the regulation of cell death, metabolism, cell division, and progenitor cell differentiation. Mitochondrial dysfunction and oxidative stress are closely associated with ischemia-reperfusion injury during organ transplantation and with different liver diseases, including cholestasis, steatosis, viral hepatitis, and drug-induced liver injury. To develop novel mitochondria-targeting therapies or interventions, a better understanding of mitochondrial dysfunction and oxidative stress in hepatic pathogenesis is very much needed. Therapies targeting mitochondria impairment and oxidative imbalance in liver diseases have been extensively studied in preclinical and clinical research. In this review, we provide an overview of how oxidative stress and mitochondrial dysfunction affect liver diseases and liver transplantation. Furthermore, we summarize recent developments of antioxidant and mitochondria-targeted interventions.

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1022 Mitochondria-Targeting Antioxidant Attenuates Carbon Tetracholride-Induced Liver Fibrosis

Cited by 9 publications

References 0 publications

Extracts from Fermented Black Garlic Exhibit a Hepatoprotective Effect on Acute Hepatic Injury

Extracts from Fermented Black Garlic Exhibit a Hepatoprotective Effect on Acute Hepatic Injury

The mitochondria‐targeted anti‐oxidant MitoQ protects against intervertebral disc degeneration by ameliorating mitochondrial dysfunction and redox imbalance

Mitochondrial Dysfunction and Oxidative Stress in Liver Transplantation and Underlying Diseases: New Insights and Therapeutics

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