aspartate amino transferase/hypoxia

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Chronic magnesium deficiency decreases tolerance to hypoxia/reoxygenation injury in mouse heart.

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OBJECTIVE Magnesium (Mg) deficiency has been reported to be associated with the development of the metabolic syndrome, cardiovascular diseases, and sudden death. We examined the influence of chronic Mg deficiency on cardiac tolerance to hypoxia/reoxygenation injury. METHODS Mice were fed an

[Effects of chronic intermittent hypoxia on hepatic function and protective mechanism of adiponectin in rats].

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Objective: To explore the effect of chronic intermittent hypoxia (CIH) on rats hepatic function, and the protective mechanism of adiponectin (Ad). Methods: Sixty healthy male wistar rats were randomly divided into 4 groups: normal control (NC), NC+ Ad, CIH, and CIH+ Ad groups with 15 rats in each.

Glycine prevents alcohol-induced liver injury by decreasing alcohol in the rat stomach.

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OBJECTIVE Inactivation of Kupffer cells prevents alcohol-induced liver injury, and hypoxia subsequent to a hypermetabolic state caused by activated Kupffer cells probably is involved in the mechanism. Glycine is known to prevent hepatic reperfusion injury. The purpose of this study was to determine

Murine glutathione S-transferase A1-1 in sickle transgenic mice.

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Patients with sickle cell anemia exhibit mild to moderate renal and liver damage. Glutathione S-transferase A1-1 is produced during kidney and liver damage. We hypothesized that cellular damage in sickle transgenic mice would lead to increased serum and urine murine glutathione S-transferase A1-1

The role of amino acid catabolism in the formation of the tricarboxylic acid cycle intermediates and ammonia in anoxic rat heart.

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Amino acid catabolism, the tricarboxylic acid cycle intermediates and ammonia formation were studied in isolated perfused rat heart under anoxia. The total net anaplerosis due to amino acid degradation in anoxia was equal to that in oxygenation (6.29 and 6.09 mumol/g dry weight per h, respectively)

[Enzymatic activity of the cerebrospinal fluid in patients with cerebral infarct].

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Dynamic measurements in the cerebrospinal fluid (CSF) of the activities of lactate dehydrogenase (LDH), its first isoenzyme (LDH1), aspartate amino transferase (AsAT), alanine amino transferase (AlAT), creatine phosphokinase (CPK), gamma-glutamyl transpeptidase (GGT) and alkaline phosphatases (ALP)

MTMR14 protects against hepatic ischemia-reperfusion injury through interacting with AKT signaling in vivo and in vitro

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Hepatic ischemia-reperfusion (IR) injury is characterized by severe inflammation and cell death. However, very few effective therapies are presently available for hepatic IR injury treatment. Here, we reported a protective function and the underlying mechanism of myotubularin-related protein 14

Interferon regulatory factor 9 is a key mediator of hepatic ischemia/reperfusion injury.

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OBJECTIVE Hepatic ischemia/reperfusion (I/R) injury is characterized by anoxic cell injury and the generation of inflammatory mediators, leading to hepatic parenchymal cell death. The activation of interferon regulatory factors (IRFs) has been implicated in hepatic I/R injury, but the role of IRF9

Exosomes derived from human umbilical cord blood mesenchymal stem cells improve hepatic ischemia reperfusion injury via delivering miR-1246.

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The purpose of this study was to explore the associated mechanism by which MSCs-derived exosomes exerted protective effect in hepatic ischemia/reperfusion injury (IRI). Human umbilical cord blood mesenchymal stem cells (hUCB-MSCs)-derived exosomes were administrated into LO2 cells exposed to

Alda-1, an ALDH2 activator, protects against hepatic ischemia/reperfusion injury in rats via inhibition of oxidative stress.

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Previous studies have proved that activation of aldehyde dehydrogenase two (ALDH2) can attenuate oxidative stress through clearance of cytotoxic aldehydes, and can protect against cardiac, cerebral, and lung ischemia/reperfusion (I/R) injuries. In this study, we investigated the effects of the ALDH2

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