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1. ミトコンドリアミオパシー：臨床的特徴および診断 mitochondrial myopathies clinical features and diagnosis
2. HIVヌクレオシド系逆転写酵素阻害剤のミトコンドリア毒性 mitochondrial toxicity of hiv nucleoside reverse transcriptase inhibitors
3. 全身疾患と関連した遺伝性ニューロパチー hereditary neuropathies associated with generalized disorders
4. 代謝性ミオパチーへのアプローチ approach to the metabolic myopathies
5. 新生児胆汁うっ滞の原因 causes of neonatal cholestasis

English Journal

Protective effects of dioscin against alcohol-induced liver injury.

Xu T1, Zheng L, Xu L, Yin L, Qi Y, Xu Y, Han X, Peng J.Author information 1College of Pharmacy, Dalian Medical University, 9 Western Lvshun South Road, Dalian, 116044, China.AbstractOur previous studies have shown that dioscin has protective effect against liver injury. However, the action of the compound against ethanol-induced liver injury is still unknown. In the present paper, ethanol-induced acute and chronic liver damage rat models were used, and the results showed that dioscin significantly alleviated liver steatosis, reduced the levels of alanine aminotransferase, aspartate aminotransferase, total triglyceride (TG), total cholesterol and malondialdehyde, and increased the levels of high-density lipoprotein, superoxide dismutase, glutathione and glutathione peroxidase. Transmission electron microscopy and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assays showed that dioscin prevented mitochondrial ultrastructural alterations and apoptosis caused by ethanol. In addition, dioscin significantly inhibited ethanol-induced cytochrome P450 2E1 activation, down-regulated the levels of mitogen-activated protein kinases phosphorylation, inhibited the expressions of nuclear factor kappa B, glucose regulated protein 78, activating transcription factor 6 and alpha subunit of translation initiation factor 2 to attenuate oxidative damage, decreased the expressions of tumor necrosis factor alpha and interleukin-6, and down-regulated the expressions of apoptosis-related proteins including p53, caspase-3, caspase-9, poly (ADP-ribose)-polymerase and cytokeratin-18. Further investigation indicated that dioscin markedly increased the expressions of peroxisome proliferators-activated receptor α and its target genes including medium-chain acyl-CoA dehydrogenase, carnitine palmitoyl-CoA transferase I and acyl-CoA oxidase to advance fatty acid β-oxidation, up-regulated the expressions of acyl-CoA synthetase long-chain family member 1, acyl-CoA synthetase long-chain family member 5, alpha-aminoadipic semialdehyde dehydrogenase and acyl-CoA dehydrogenase to promote fatty acid metabolism, and down-regulated the expressions of glycerol-3-phosphate acyltransferase, diacylglycerol acyltransferase 1 and diacylglycerol acyltransferase 2 to accelerate TG synthesis. However, dioscin had no effects on the expressions of sterol regulatory element-binding protein-1c, fatty acid synthase, acetyl-CoA carboxylase 1 and stearoyl-CoA desaturase 1 associated with fatty acid synthesis. In conclusion, dioscin shows excellent protective effect against ethanol-induced liver injury through ameliorating ethanol-induced oxidative stress, mitochondrial function, inflammatory cytokine production, apoptosis and liver steatosis, which should be developed as a new drug for the treatment of ethanol-induced liver injury in the future.
Archives of toxicology.Arch Toxicol.2014 Mar;88(3):739-53. doi: 10.1007/s00204-013-1148-8. Epub 2013 Oct 22.
Our previous studies have shown that dioscin has protective effect against liver injury. However, the action of the compound against ethanol-induced liver injury is still unknown. In the present paper, ethanol-induced acute and chronic liver damage rat models were used, and the results showed that d
PMID 24146112

Proteomic analysis of post-nuclear supernatant fraction and percoll-purified membranes prepared from brain cortex of rats exposed to increasing doses of morphine.

Ujcikova H, Eckhardt A, Kagan D, Roubalova L, Svoboda P.AbstractBACKGROUND: Proteomic analysis was performed in post-nuclear supernatant (PNS) and Percoll-purified membranes (PM) prepared from fore brain cortex of rats exposed to increasing doses of morphine (10-50 mg/kg) for 10 days.
Proteome science.Proteome Sci.2014 Feb 14;12(1):11. [Epub ahead of print]
BACKGROUND: Proteomic analysis was performed in post-nuclear supernatant (PNS) and Percoll-purified membranes (PM) prepared from fore brain cortex of rats exposed to increasing doses of morphine (10-50 mg/kg) for 10 days.RESULTS: In PNS, the 10 up ([upwards arrow])- or down ([downwards arrow])-regul
PMID 24528483

Hepatoprotective properties of sesamin against CCl4 induced oxidative stress-mediated apoptosis in mice via JNK pathway.

Ma JQ1, Ding J2, Zhang L2, Liu CM3.Author information 1School of Chemistry and Pharmaceutical, Sichuan University of Science and Engineering, 643000 Zigong City, Sichuan Province, PR China. Electronic address: a1032042419@126.com.2School of Chemistry and Pharmaceutical, Sichuan University of Science and Engineering, 643000 Zigong City, Sichuan Province, PR China.3School of Life Science, Jiangsu Normal University, No. 101, Shanghai Road, Tongshan New Area, Xuzhou City 221116, Jiangsu Province, PR China.AbstractSesamin (Ses), one of the major lignan derived from sesame seeds, has been reported to have many benefits and medicinal properties. However, its protective effects against carbon tetrachloride (CCl4) induced injury in liver have not been clarified. The aim of the present study was to investigate the hepatoprotective effects of sesamin on oxidative stress and apoptosis in mice exposed to CCl4. Our data showed that sesamin significantly prevented CCl4-induced hepatotoxicity in a dose-dependent manner, indicated by both diagnostic indicators of liver damage (serum aminotransferase activities) and histopathological analysis. Moreover, CCl4-induced profound elevation of reactive oxygen species (ROS) production and oxidative stress, as evidenced by increasing of lipid peroxidation level and depleting of the total antioxidant capacity (TAC) in liver, were suppressed by treatment with sesamin. Furthermore, TUNEL assay showed that CCl4-induced apoptosis in mouse liver was significantly inhibited by sesamin. In exploring the underlying mechanisms of sesamin action, we found that activities of caspase-3 were markedly inhibited by the treatment of sesamin in the liver of CCl4 treated mice. Sesamin increased expression levels of phosphorylated Jun N-terminal kinases (JNK) in liver, which in turn inactivated pro-apoptotic signaling events restoring the balance between mitochondrial pro- and anti-apoptotic Bcl-2 proteins and decreasing the release of mitochondrial cytochrome c in liver of CCl4 treated mice. JNK was also involved in the mitochondrial extrinsic apoptotic pathways of sesamin effects against CCl4 induced liver injury by regulating the expression levels of phosphorylated c-Jun proteins, necrosis factor-alpha (TNF-α) and Bak. In conclusion, these results suggested that the inhibition of CCl4-induced apoptosis by sesamin is due at least in part to its anti-oxidant activity and its ability to modulate the JNK signaling pathway.
Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association.Food Chem Toxicol.2014 Feb;64:41-8. doi: 10.1016/j.fct.2013.11.017. Epub 2013 Nov 25.
Sesamin (Ses), one of the major lignan derived from sesame seeds, has been reported to have many benefits and medicinal properties. However, its protective effects against carbon tetrachloride (CCl4) induced injury in liver have not been clarified. The aim of the present study was to investigate the
PMID 24287204

Japanese Journal

Recombinant expression, purification and crystallographic studies of the mature form of human mitochondrial aspartate aminotransferase

BioScience Trends 10(1), 79-84, 2016
NAID 130005133312

Recombinant expression, purification and crystallographic studies of the mature form of human mitochondrial aspartate aminotransferase

BioScience Trends advpub(0), 2016
NAID 130005129189

Tacrine, an Oral Acetylcholinesterase Inhibitor, Induced Hepatic Oxidative Damage, Which Was Blocked by Liquiritigenin through GSK3-beta Inhibition

Biological and Pharmaceutical Bulletin 38(2), 184-192, 2015
NAID 130004872247

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★リンクテーブル★

リンク元	「ミトコンドリア型アスパラギン酸アミノ基転移酵素」
関連記事	「aspartate」「mitochondrial」「aspartate aminotransferase」「aminotransferase」