Dexamethasone improves heat stroke-induced multiorgan dysfunction and damage in rats.

Dexamethasone (DXM) is known as an immunosuppressive drug used for inflammation control. In the present study, we attempted to examine whether DXM administration could attenuate the hypercoagulable state and the overproduction of pro-inflammatory cytokines, improve arterial hypotension, cerebral ischemia and damage, and vital organ failure in a rat model of heat stroke. The results indicated that all the rats suffering from heat stroke showed high serum levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), accompanied with increased prothrombin time, activated partial thromboplastin time and D-D dimer, and decreased protein C.

Chronic exposure to Rhodobacter sphaeroides extract Lycogen™ prevents UVA-induced malondialdehyde accumulation and procollagen I down-regulation in human dermal fibroblasts.

UVA contributes to the pathogenesis of skin aging by downregulation of procollagen I content and induction of matrix metalloproteinase (MMP)-associated responses. Application of antioxidants such as lycopene has been demonstrated as a convenient way to achieve protection against skin aging. Lycogen™, derived from the extracts of Rhodobacter sphaeroides, exerts several biological effects similar to that of lycopene whereas most of its anti-aging efficacy remains uncertain.

Inhibition of Epstein-Barr virus lytic cycle by an ethyl acetate subfraction separated from Polygonum cuspidatum root and its major component, emodin.

Polygonum cuspidatum is widely used as a medicinal herb in Asia. In this study, we examined the ethyl acetate subfraction F3 obtained from P. cuspidatum root and its major component, emodin, for their capacity to inhibit the Epstein-Barr virus (EBV) lytic cycle.

Attenuation of circulatory shock and cerebral ischemia injury in heat stroke by combination treatment with dexamethasone and hydroxyethyl starch.

Background: Increased systemic cytokines and elevated brain levels of monoamines, and hydroxyl radical productions are thought to aggravate the conditions of cerebral ischemia and neuronal damage during heat stroke. Dexamethasone (DXM) is a known immunosuppressive drug used in controlling inflammation, and hydroxyethyl starch (HES) is used as a volume-expanding drug in cerebral ischemia and/or cerebral injury. Acute treatment with a combined therapeutic approach has been repeatedly advocated in cerebral ischemia experiments.

Effects of combination treatment with dexamethasone and mannitol on neuronal damage and survival in experimental heat stroke.

There is evidence that increased plasma cytokines, elevated brain levels of monoamines and hydroxyl radical production may be implicated in pathogenesis during heat stroke in rats. Acute treatment with a combined therapeutic approach has been repeatedly advocated in cerebral ischemia experiments. The aim of this study was to investigate whether the combined agent (mannitol and dexamethasone) has beneficial efficacy to improve the survival time (ST) and heat stroke-induced damage in experimental heat stroke.

Effects of S-adenosylhomocysteine and homocysteine on DNA damage and cell cytotoxicity in murine hepatic and microglia cell lines.

Limited research has been performed on S-adenosylhomocysteine (SAH) or homocysteine (Hcy)-evoked cell damage in hepatic and neuronal cells. In this study, we assessed effects of SAH or Hcy on cell cytotoxicity and DNA damage in hepatic and neuronal cells and attempted to find the underlying mechanism. Cell cytotoxicity and DNA damage were evaluated in murine hepatic cells (BNL CL.

Synergistic effects of S-adenosylhomocysteine and homocysteine on DNA damage in a murine microglial cell line.

Background: Homocysteine (Hcy) and S-adenosylhomocysteine (SAH) are 2 major metabolites of methionine. However, little is known about their interactions in human diseases.

Methods: We determined the interaction of Hcy with SAH on DNA damage (measured as comet formation) and DNA hypomethylation (assayed as 5-methyldeoxycytidine, 5-mdc) in BV-2 cells (immortalized murine microglia).

Intracellular levels of S-adenosylhomocysteine but not homocysteine are highly correlated to the expression of nm23-H1 and the level of 5-methyldeoxycytidine in human hepatoma cells with different invasion activities.

Cellular methylation imbalance is associated with tumor progression, hepatic cancer, and cardiovascular disease. S-Adenosylhomocysteine (SAH) is an inhibitor of cellular methyltransferases, and increasing evidence suggests that SAH rather than homocysteine (Hcy) plays a crucial role in mediating these disorders related to methylation imbalance. The anti-metastatic gene nm23-H1 was recently identified in murine and human cancer lines, and the expressions of nm23-H1 mRNA and protein have been shown to be useful tumor invasion markers.

Various forms of homocysteine and oxidative status in the plasma of ischemic-stroke patients as compared to healthy controls.

Objectives: We compared various forms of plasma homocysteine (Hcy) including total Hcy (tHcy), free reduced Hcy (reHcy), free oxidized Hcy (oxHcy) and reHcy plus oxHcy between patients with acute/subacute-ischemic stroke and healthy controls. We also investigated whether the patients have increased oxidative stress.

Design And Methods: Using an in-tube derivatization method, we measured plasma levels of tHcy, reHcy and oxHcy in 55 ischemic-stroke patients (14 females and 41 males, median age 64) and 52 age-matched healthy subjects (15 females and 37 males, median age 60).

S-adenosylhomocysteine enhances hydrogen peroxide-induced DNA damage by inhibition of DNA repair in two cell lines.

It has been proposed that hyperhomocysteinemia may exert its pathogenic effects largely through metabolic accumulation of S-adenosylhomocysteine (SAH), a strong noncompetitive inhibitor of most methyltransferases. Here, we investigated the effects of SAH on H(2)O(2)-induced cellular DNA damage in comparison with the effects of homocysteine (Hcy) in a mouse endothelial cell line and a human intestinal cell line. Cells were preincubated for 2 h with H(2)O(2) (20 microM) followed by incubation with SAH or Hcy for 3 h.