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Dihydrotestosterone (DHT) differentially affects cerebral vascular inflammation in normoxia and hypoxia
Rayna J Gonzales, Diana N Krause and Sue P Duckles
Pharmacology, University of California Irvine School of Medicine, Med Surg II, Irvine, CA, 92697
ABSTRACT
Sex steroids significantly impact the severity and outcome of cardiovascular disease, and vascular inflammation is increasingly recognized as a key element in the pathophysiology of ischemic stroke. Past studies have shown that testosterone augments the inflammatory response in cerebral blood vessels. Therefore, we investigated the effect of the more potent metabolite of testosterone, DHT, on inflammatory pathways in the cerebral vasculature during hypoxia. Cerebral arteries were isolated from castrated male rats treated with DHT in vivo (3 wk) or isolated from castrated male rats exposed to DHT (10 nM) in vitro. Nuclear NFB activation was increased by in vitro hypoxia (1%; 1 to 6 hr) compared to normoxia; this response was blunted by DHT (10 nM). In normoxia, COX-2 protein was higher in arteries treated with DHT (in vitro or in vivo) compared to vehicle. Hypoxia augmented COX-2 levels, but this increase was suppressed by DHT (in vitro or in vivo). Thus, DHT, by increasing COX-2 in normoxic conditions, contributes to a state of vascular inflammation. In contrast, during hypoxia, DHT suppressed NFB activity and COX-2. Thus, androgens may have a differential impact on regulation of inflammation during pathophysiological compared to normal physiological conditions. AHA National Scientist Development Grant (RJG).
Dihydrotestosterone (DHT) differentially affects cerebral vascular inflammation in normoxia and hypoxia
Rayna J Gonzales, Diana N Krause and Sue P Duckles
Pharmacology, University of California Irvine School of Medicine, Med Surg II, Irvine, CA, 92697
ABSTRACT
Sex steroids significantly impact the severity and outcome of cardiovascular disease, and vascular inflammation is increasingly recognized as a key element in the pathophysiology of ischemic stroke. Past studies have shown that testosterone augments the inflammatory response in cerebral blood vessels. Therefore, we investigated the effect of the more potent metabolite of testosterone, DHT, on inflammatory pathways in the cerebral vasculature during hypoxia. Cerebral arteries were isolated from castrated male rats treated with DHT in vivo (3 wk) or isolated from castrated male rats exposed to DHT (10 nM) in vitro. Nuclear NFB activation was increased by in vitro hypoxia (1%; 1 to 6 hr) compared to normoxia; this response was blunted by DHT (10 nM). In normoxia, COX-2 protein was higher in arteries treated with DHT (in vitro or in vivo) compared to vehicle. Hypoxia augmented COX-2 levels, but this increase was suppressed by DHT (in vitro or in vivo). Thus, DHT, by increasing COX-2 in normoxic conditions, contributes to a state of vascular inflammation. In contrast, during hypoxia, DHT suppressed NFB activity and COX-2. Thus, androgens may have a differential impact on regulation of inflammation during pathophysiological compared to normal physiological conditions. AHA National Scientist Development Grant (RJG).