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2 3 dihydroxybenzoic acid/necrosis

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We induced acute skeletal muscle necrosis in rats using bupivacaine hydrochloride and found that both 2,5- and 2,3-dihydroxybenzoic acid significantly increased in skeletal muscle. A single administration of dimethyl sulphoxide, a free radical scavenger, significantly lowered concentrations of 2,5-

[Dimethyl sulphoxide suppresses hydroxyl radical formation of muscle fiber necrosis induced by bupivacaine hydrochloride].

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We induced acute skeletal muscle necrosis by using bupivacaine hydrochloride in Wistar rats and found that both 2,5- and 2, 3-dihydroxybenzoic acid significantly increased in the skeletal muscle. Dimethyl sulphoxide, a free radical scavenger, was administrated for 5 days, and resulted in significant
Chronic hyperglycaemia and inflammation are present in diabetes and both processes have been related to the pathogenesis of diabetic kidney disease. Epicatechin (EC) and main colonic phenolic acids derived from flavonoid intake, such as 2,3-dihydroxybenzoic acid (DHBA), 3,4-dihydroxyphenylacetic

Hydroxyl radical generation, levels of tumor necrosis factor-alpha, and progression to heart failure after acute myocardial infarction.

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OBJECTIVE We used acetylsalicylic acid (ASA) as a probing agent to quantify hydroxyl radical ((*)OH) in Controls and patients with coronary artery disease and to prospectively investigate (*)OH production in patients with myocardial infarction (MI) complicated by heart failure
The proliferation and migration of vascular smooth muscle cells (VSMCs) play important roles in the formation and progression of intimal thickening in early-phase atherosclerosis and in restenosis after vascular injury. Tumor necrosis factor-α (TNF-α) is released from macrophages in atherosclerotic
HHP (hypobaric hypoxia preconditioning) induces the overexpression of HSP70 (heat-shock protein 70), as well as tolerance to cerebral ischaemia. In the present study, we hypothesized that HHP would protect against HAE (high-altitude exposure)-induced acute lung injury and oedema via promoting the

Activated protein C improves heatstroke outcomes through restoration of normal hypothalamic and thermoregulatory function.

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BACKGROUND Human recombinant activated protein C (APC) has been found to be beneficial in treating heatstroke in both humans and rats. Here, we further investigated the possible mechanism underlying the therapeutic action exerted by APC in experimental heatstroke. METHODS Unanesthetized and

Oxidative stress causes nuclear factor-kappaB activation in acute hypovolemic hemorrhagic shock.

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Nuclear Factor kappaB (NFkappaB) is an ubiquitous rapid response transcription factor involved in inflammatory reactions and exerts its action by expressing cytokines, chemokines, and cell adhesion molecules. We investigated the role of NF-kappaB in acute hypovolemic hemorrhagic (Hem) shock. Hem

Melatonin reduces acute lung inflammation, edema, and hemorrhage in heatstroke rats.

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OBJECTIVE To assess the therapeutic effect of melatonin on heat-induced acute lung inflammation and injury in rats. METHODS Heatstroke was induced by exposing anesthetized rats to heat stress (36 °C, 100 min). Rats were treated with vehicle or melatonin (0.2, 1, 5 mg/kg) by intravenous
We studied the effects of the aminosteroid U-74389G (21-[4-(2, 6-di-1-pyrrolidinyl-4-pyrimidinyl)-1-piperazinyl]-pregna-1,4,9(11)- triene-3,20-dione(2)-2-butenenedionate), a putative inhibitor of lipid peroxidation, which protects the rat myocardium after ischemia and reperfusion.

Hypoxic preconditioning attenuated in kainic acid-induced neurotoxicity in rat hippocampus.

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The neuroprotective effect of hypoxic preconditioning on kainate (KA)-induced neurotoxicity, including apoptosis and necrosis, was investigated in rat hippocampus. Female Wistar-Kyoto rats were subjected to 380 mm Hg in an altitude chamber for 15 h/day for 28 days. Intrahippocampal infusion of KA
OBJECTIVE The primary goal of this study was to test whether high-altitude exposure (HAE: 0.9% O(2) at 0.47 ATA for 24 hours) was capable of increasing the systemic inflammatory markers as well as the toxic organ injury indicators in rats, with a secondary goal to test whether preinduction of heat

Resuscitation from experimental heatstroke by brain cooling therapy.

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We have used hypothermic retrograde jugular venous flush to cool the brain previously and to provide better resuscitation than peripheral cold saline infusion during heatstroke in the rat. The current study was performed to assess the effects of brain cooling further on production of reactive

Decrease of heatstroke-induced multiorgan dysfunction by whole body cooling in streptozotocin-induced diabetic rats.

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The present study was conducted to assess the effects of whole body cooling on multiorgan dysfunction that occurred during heatstroke in streptozotocin (STZ)-induced diabetic rats. The rats were randomly divided into four groups: [1] the normal control, [2] diabetic control, [3] diabetic heatstroke,

Attenuating brain inflammation, ischemia, and oxidative damage by hyperbaric oxygen in diabetic rats after heat stroke.

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OBJECTIVE Alternating hypothalamic-pituitary-adrenal axis mechanisms would lead to multiple organs dysfunction or failure. Herein, we attempt to assess whether hypothalamic inflammation and ischemic and oxidative damage that occurred during heatstroke (HS) can be affected by hyperbaric oxygen (HBO₂)
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