Arundic Acid (ONO-2506), an Inhibitor of S100B Protein Synthesis, Prevents Neurological Deficits and Brain Tissue Damage Following Intracerebral Hemorrhage in Male Wistar Rats

Excessive alcohol consumption can lead to brain tissue damage and cognitive dysfunction. It has been shown that heavy drinking is associated with an earlier onset of neurodegenerative diseases such as Alzheimer’s disease. Acetaldehyde, the most toxic metabolite of ethanol, is speculated to mediate the brain tissue damage and cognitive dysfunction induced by the chronic excessive consumption of alcohol. However, the exact mechanisms by which acetaldehyde induces neurotoxicity are not totally understood. In this study, we investigated the cytotoxic effects of acetaldehyde in SH-SY5Y cells and found that acetaldehyde induced apoptosis of SH-SY5Y cells by downregulating the expression of antiapoptoticBcl-2andBcl-xLand upregulating the expression of proapoptoticBax. Acetaldehyde treatment led to a significant decrease in the levels of activated Akt and cyclic AMP-responsive element binding protein (CREB). In addition, acetaldehyde induced the activation of p38 mitogen-activated protein kinase (MAPK) while inhibiting the activation of extracellular signal-regulated kinases (ERKs, p44/p42MAPK). Meanwhile, acetaldehyde treatment caused an increase in the production of reactive oxygen species and elevated the oxidative stress in SH-SY5Y cells. Therefore, acetaldehyde induces cytotoxicity of SH-SY5Y cells via promotion of apoptotic signaling, inhibition of cell survival pathway, and induction of oxidative stress.

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Piezosurgery prevents brain tissue damage: an experimental study on a new rat model

International Journal of Oral and Maxillofacial Surgery ◽

10.1016/j.ijom.2011.05.008 ◽

2011 ◽

Vol 40 (8) ◽

pp. 840-844 ◽

Cited By ~ 12

Author(s):

G. Pavlíková ◽

R. Foltán ◽

M. Burian ◽

E. Horká ◽

S. Adámek ◽

...

Keyword(s):

Experimental Study ◽

Brain Tissue ◽

Rat Model ◽

Tissue Damage ◽

Brain Tissue Damage

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Pre-existing inflammatory state compromises heat tolerance in rats exposed to heat stress

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00921.2005 ◽

2007 ◽

Vol 292 (1) ◽

pp. R186-R194 ◽

Cited By ~ 27

Author(s):

Chin Leong Lim ◽

Gary Wilson ◽

Lindsay Brown ◽

Jeff S. Coombes ◽

Laurel T. Mackinnon

Keyword(s):

Heat Stress ◽

Heat Tolerance ◽

Tissue Damage ◽

Wistar Rats ◽

Heat Stroke ◽

Heat Exposure ◽

The Core ◽

Male Wistar Rats ◽

Inflammatory State ◽

Severe Heat Stress

This study investigated the roles of endotoxemia and heat-induced tissue damage in the pathology of heat stroke. In groups of eight, male Wistar rats were treated with heat exposure only (HE), or heat exposure with turpentine (T+HE), dexamethasone (D+HE), and turpentine and dexamethasone combined (TD+HE). The rats remained sedated for 2 h after receiving the respective treatments, followed by heat exposure until the core temperature (Tc) was 42°C for 15 min; control rats received turpentine (T), dexamethasone (D), and turpentine and dexamethasone (TD) without heat stress. Blood samples were collected before treatment ( baseline I), after 2 h of passive rest ( baseline II), at Tc 40°C (T40), and 15 min after achieving Tc 42°C (T42). No rats died in the nonheat-stressed groups. Survival rate was lowest in the TD+HE rats (37.5%), followed by the HE (62.5%), T+HE (75%), and D+HE (100%) rats ( P < 0.05). The duration of survival at T42°C was shortest in the TD+HE rats (9.9 ± 6.2 min) ( P < 0.01), followed by the T+HE (11.3 ± 6.1 min) and the HE (12.2 ± 4 min) ( P < 0.05) rats. The increase in plasma IL-6 concentrations was highest in the T+HE (352%) and HE (178%) rats ( P < 0.05). D+HE treatment suppressed the increases in plasma aspartate transaminase, alanine aminotransferase, and IL-6 and LPS concentrations during severe heat stress. Heat stroke can be triggered by endotoxemia or heat-induced tissue damage, and preexisting inflammation compromises heat tolerance, whereas blocking endotoxemia increases heat tolerance.

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