کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8338945 | 1541012 | 2013 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Nongenomic bronchodilating action elicited by dehydroepiandrosterone (DHEA) in a guinea pig asthma model
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
SOCEDHEAReceptor-operated Ca2+ channelROCCVDCCKHsEmaxDHEA-SCCHdehydroepiandrosteroneASMOVAIC50KClDMSO - DMSOl-NAME - L-NAMENω-nitro-l-arginine methyl ester - N-Nitro-L-Arginine Methyl EsterAsthma - آسمmaximal effect - اثر حداکثرAdrenal steroid - استروئید آدنالOvalbumin - اوبلبومینbradykinin - برادیکینینDimethylsulfoxide - دیمتیل سولفواکسیدdehydroepiandrosterone sulfate - سولفات dehydroepiandrosteroneAirway smooth muscle - عضله صاف راه هواییinhibitory concentration 50 - غلظت مهاری 50Lar - لارLung resistance - مقاومت ریهNitric oxide - نیتریک اکسیدEarly asthmatic response - واکنش زودرس آسمStore-operated Ca2+ entry - ورودی Ca2 + ذخیره شدهLate asthmatic response - پاسخ کوتاه مدت آسمCarbachol - کارباکولVoltage-dependent Ca2+ channels - کانال Ca2 + وابسته به ولتاژPotassium chloride - کلرید پتاسیمEAR - گوش
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Nongenomic bronchodilating action elicited by dehydroepiandrosterone (DHEA) in a guinea pig asthma model Nongenomic bronchodilating action elicited by dehydroepiandrosterone (DHEA) in a guinea pig asthma model](/preview/png/8338945.png)
چکیده انگلیسی
Primates secrete large amounts of the precursor steroid dehydroepiandrosterone (DHEA); in humans, its levels are low during childhood and start declining after the fourth decade. It has been postulated that the progressive decline in DHEA levels may be related with the severity of asthma associated with age. To determine whether DHEA may regulate the airway smooth muscle (ASM) activity, isolated tracheal rings with and without epithelium from male guinea pigs were isometrically recorded to characterize the response of ASM to DHEA at different concentrations on KCl- and carbachol (CCh)-induced contraction as well as on ovalbumin (OVA)-induced contraction in sensitized guinea pigs. Additionally, we used barometric plethysmography in sensitized guinea pigs in order to compare changes of the lung resistance increased by the antigen challenge to OVA in the absence and presence of different doses of DHEA. DHEA concentration-dependently abolished the contraction to KCl, CCh and OVA, and no differences were found in preparations with and without epithelium. DHEA-induced relaxation was not modified by the suppression of protein synthesis or transcription, pharmacological inhibition of nitric oxide (NO) synthase, nor by antagonist of β2-adrenergic receptors or an inhibitor of the 3β-HSD enzyme. Likewise, Ca2+-induced contraction in Ca2+-free depolarized tissues was antagonized by DHEA, and the contraction to the L-type voltage-dependent calcium channel activator (Bay K 8644) was inhibited by DHEA. Furthermore, DHEA prevented OVA-induced increases in lung resistance. These results indicate that DHEA-induced relaxation in ASM is a nongenomic (membrane) action and is not produced after its bioconversion. The data suggest that DHEA-induced relaxation is an epithelium- and NO-independent mechanism that involves a blockade of voltage-dependent calcium channels and possible non-selective cation channels.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: The Journal of Steroid Biochemistry and Molecular Biology - Volume 138, November 2013, Pages 174-182
Journal: The Journal of Steroid Biochemistry and Molecular Biology - Volume 138, November 2013, Pages 174-182
نویسندگان
Julia Espinoza, Luis M. Montaño, Mercedes PerusquÃa,