Abstract：
OBJECTIVE: Bell\'s palsy, also referred to as clinical manifestations of unilateral facial nerve palsy, encompasses downward angling of the corners of the mouth, the absence of forehead creases, and unilateral incomplete eyelid closure. The incidence of Bell\'s palsy has increased progressively in recent years, but the underlying mechanism of its occurrence remains unknown; therefore, it is essential to investigate both the cause and treatment of Bell\'s palsy. Member 2 of the Subfamily V Transient Receptor Potential Cation Channel is a mechanically and thermally sensitive ion channel that plays a crucial role in neural growth and development. Using a novel modeling technique, we endeavored to develop an animal model of Bell\'s palsy and determine whether TRPV2 expression is altered throughout the course of a facial nerve injury.
METHODS: The rats were categorized into 3 groups, and their facial nerve function was assessed using RT-qPCR, WB, and pathologic testing, respectively, after undergoing unilateral cold air stimulation for 1, 3, and 7 days. TRPV2 expression was identified using these techniques.
RESULTS: In response to cold stimulation, rats exhibited facial nerve paralysis symptoms, demyelinating lesions in the facial nerve, and increased TRPV2 expression.
CONCLUSIONS: Extended cold stimulation of the facial nerve in rats may lead to an imbalance in facial nerve homeostasis and increased TRPV2 expression. These findings will contribute to the understanding of the potential mechanism by which cold stimulation affects the facial nerve. Moreover, this finding implies that TRPV2 could possibly function as an additional diagnostic marker or therapeutic target in the context of Bell\'s palsy.
METHODS: The rats were categorized into 3 groups, and their facial nerve function was assessed using RT-qPCR, WB, and pathologic testing, respectively, after undergoing unilateral cold air stimulation for 1, 3, and 7 days. TRPV2 expression was identified using these techniques.
RESULTS: In response to cold stimulation, rats exhibited facial nerve paralysis symptoms, demyelinating lesions in the facial nerve, and increased TRPV2 expression.
CONCLUSIONS: Extended cold stimulation of the facial nerve in rats may lead to an imbalance in facial nerve homeostasis and increased TRPV2 expression. These findings will contribute to the understanding of the potential mechanism by which cold stimulation affects the facial nerve. Moreover, this finding implies that TRPV2 could possibly function as an additional diagnostic marker or therapeutic target in the context of Bell\'s palsy.
摘要：
目的：贝尔麻痹，也称为单侧面神经麻痹的临床表现，包括嘴角的向下倾斜，没有额头折痕，单侧眼睑闭合不全。近年来，贝尔麻痹的发病率逐渐增加，但其发生的潜在机制仍然未知；因此，研究贝尔氏麻痹的病因和治疗方法至关重要。亚家族V瞬时受体电位阳离子通道的成员2是机械和热敏感的离子通道，在神经生长和发育中起着至关重要的作用。使用一种新颖的建模技术，我们致力于建立贝尔麻痹的动物模型，并确定TRPV2表达是否在整个面神经损伤过程中发生改变。
方法：将大鼠分为3组，使用RT-qPCR评估他们的面神经功能，WB,和病理测试，分别,在接受单侧冷空气刺激1、3和7天后。使用这些技术鉴定TRPV2表达。
结果：响应冷刺激，大鼠表现出面神经麻痹症状，面神经脱髓鞘病变,TRPV2表达增加。
结论：大鼠面神经的延长冷刺激可能导致面神经稳态失衡和TRPV2表达增加。这些发现将有助于理解冷刺激影响面神经的潜在机制。此外，这一发现暗示TRPV2可能作为贝尔麻痹的额外诊断标记物或治疗靶点发挥作用.
方法：将大鼠分为3组，使用RT-qPCR评估他们的面神经功能，WB,和病理测试，分别,在接受单侧冷空气刺激1、3和7天后。使用这些技术鉴定TRPV2表达。
结果：响应冷刺激，大鼠表现出面神经麻痹症状，面神经脱髓鞘病变,TRPV2表达增加。
结论：大鼠面神经的延长冷刺激可能导致面神经稳态失衡和TRPV2表达增加。这些发现将有助于理解冷刺激影响面神经的潜在机制。此外，这一发现暗示TRPV2可能作为贝尔麻痹的额外诊断标记物或治疗靶点发挥作用.
