สืบค้นงานวิจัย
TRPV1 and TRPA1 channel function following streptozotocin-induced diabetes in rats
Teeraporn Katisart - ไม่ระบุหน่วยงาน
ชื่อเรื่อง (EN): TRPV1 and TRPA1 channel function following streptozotocin-induced diabetes in rats
ผู้แต่ง / หัวหน้าโครงการ (EN): Teeraporn Katisart
บทคัดย่อ (EN): The aim of this study is to study the change in TRV1 and TRPA1 channel responses with time following the treatment with streptozotocin. The results showed that as early as 36 hours after induction of diabetes by STZ, the contractile responses to capsaicin were significantly reduced in comparison to those of the controls and this reduction persisted until the eight weeks time point. In contrast, responses to the TRPA1 agonist allyl isothiocyanate were not affected at early time points but were reduced one week after STZ treatment. This detailed time course analysis suggests that there are novel mechanisms of modulation of the TRPV1 channels in this STZ model. In conclusion, in the rat urinary bladder or colon preparations, diabetes mellitus using STZ animal model caused the impairment caused by STZ-induced diabetes occurred very early (within 36 hours after diabetes induction) in TRPV1 channel but not TRPA1 channel. There are specific early effects of STZ treatment on TRPV1 channel function at a time when other afferent nerve terminal channels (TRPA1) are functioning normally, suggesting that early onset of dysfunction in TRPV1 signalling may not merely be the consequence of nerve damage. The mechanism of this impairment may not be the effect of neuropathy on neurotransmitter release or nerve damage. Improving the responsiveness of nerves of bladder in diabetic patients might be of therapeutic benefit. 1 Department of Biology, Mahasarakham University, 44150 Thailand 2 School of Life Science, University of Hertfordshire, AL10 9AB United Kingdom * Corresponding author: tkatisart@yahoo.com Introduction Diabetic bladder dysfunction is characterized by a triad of decreased sensation, increased capacity and poor emptying with a prevalence estimated to be between 32% and 45% (Hunter and Moore, 2003). The study in animal models of diabetes especial ly in streptozotocin induceddiabetes in rats indicated that diabetes both decreased (Longhurst and Belis, 1986) and increased detrusor contractility (Warning and Wrendt, 2000). Abnormalities of bladder function such as reduced contractile responses to nerve stimulation and applied acetylcholine have been reported (Longhurst and Belis, 1986). In addition, there are abnormalities in afferent nerve signaling in bladder from streptozotocin-induced diabetic rats (Steer et al., 1994). Transient Receptor Potential (TRP) channels are a recently identified large group of calcium permeable ion channels that allow calcium entry without requiring cell depolarization. TRPV1 is the most investigated channel compared to other TRP subfamilies. TRPV1 channel is activated by capsaicin, which has been shown to cause contraction of the rat bladder (Saitoh et al., 2007) and has been used in the treatment of neurogenic bladder dysfunction (Fowler et al., 1992). Pinna et al. (1994) have shown decreased capsaicin responses in STZ-diabetic rat bladder. TRPV1 levels are reduced in skin biopsies from patients with diabetic neuropathy (Facer et al., 2007) and insulin has been shown to cause sensitization and translocation of TRPV1 receptors (Van Buren)
บทคัดย่อ: ไม่พบข้อมูลจากหน่วยงานต้นทาง
ภาษา (EN): th
จำนวนหน้า: 6
เอกสารแนบ: https://www.semanticscholar.org/paper/TRPV-1-and-TRPA-1-channel-function-following-in-Katisart/cfcd6f14d5f357de2d4673027a06963cbf2990de
คำสำคัญ (EN): rats
หากไม่พบเอกสารฉบับเต็ม (Full Text) โปรดติดต่อหน่วยงานเจ้าของข้อมูล

การอ้างอิง

Teeraporn Katisart. "TRPV1 and TRPA1 channel function following streptozotocin-induced diabetes in rats". ไม่ระบุหน่วยงาน. 2555

Teeraporn Katisart. "TRPV1 and TRPA1 channel function following streptozotocin-induced diabetes in rats". ไม่ระบุหน่วยงาน. 2555. Print.



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TRPV1 and TRPA1 channel function following streptozotocin-induced diabetes in rats
Teeraporn Katisart
ไม่ระบุผู้เผยแพร่
2555
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