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一项评估局部普萘洛尔预防应激性脱发的单中心临床试验。

A single-center clinical trial evaluating topical propranolol for preventing stress-induced hair loss.

机构信息

School of Pharmaceutical Sciences (Shenzhen), Shenzhen Campus of Sun Yat-sen University, Shenzhen, Guangdong, P. R. China.

Plastic, Cosmetic and Burn Wound Center, The First Affiliated Hospital of Jiamusi University, Jiamusi, Heilongjiang, P. R. China.

出版信息

FASEB J. 2024 Nov 30;38(22):e70191. doi: 10.1096/fj.202401027R.

DOI:10.1096/fj.202401027R
PMID:39570058
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11580711/
Abstract

There is currently a lack of pathological research on the hair loss caused by stress, and there is no effective treatment available. It has been previously reported that stress can cause sympathetic nerve activation and release of norepinephrine, which binds to beta-2 adrenergic receptors and causes a series of chemical reactions. Propranolol, as a beta-2 adrenergic receptors blocker, competitively antagonizes the effects of norepinephrine. We initiated a single-center clinical trial with a self-controlled approach to assess the effectiveness of topical applied hydrochloride salt of propranolol solution in preventing stress-induced hair loss in humans. A total of 20 volunteers were enrolled. 14 out of 20 volunteers experienced a significant reduction in the number of hair loss (p < .05) after using hydrochloride salt of propranolol solution. No local adverse reactions were found. This study showed hydrochloride salt of propranolol solution may alleviate stress-induced alopecia to a certain extent, which provides clues for the development of pharmaceutical interventions for the treatment of stress-induced alopecia.

摘要

目前,对于压力导致的脱发的病理研究还很少,也没有有效的治疗方法。此前有报道称,压力会导致交感神经激活和去甲肾上腺素释放,去甲肾上腺素与β2 肾上腺素能受体结合,引起一系列化学反应。普萘洛尔作为β2 肾上腺素能受体阻滞剂,竞争性拮抗去甲肾上腺素的作用。我们采用自身对照的方法开展了一项单中心临床试验,评估局部应用盐酸普萘洛尔溶液预防人类应激性脱发的有效性。共招募了 20 名志愿者。20 名志愿者中有 14 名在使用盐酸普萘洛尔溶液后脱发数量明显减少(p <.05)。未发现局部不良反应。本研究表明盐酸普萘洛尔溶液可能在一定程度上缓解应激性脱发,为开发治疗应激性脱发的药物干预措施提供了线索。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8366/11580711/d6062ab2e55e/FSB2-38-e70191-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8366/11580711/5ec064c9de70/FSB2-38-e70191-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8366/11580711/6a613ddda467/FSB2-38-e70191-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8366/11580711/02868e586c0a/FSB2-38-e70191-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8366/11580711/d6062ab2e55e/FSB2-38-e70191-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8366/11580711/5ec064c9de70/FSB2-38-e70191-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8366/11580711/6a613ddda467/FSB2-38-e70191-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8366/11580711/02868e586c0a/FSB2-38-e70191-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8366/11580711/d6062ab2e55e/FSB2-38-e70191-g003.jpg

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本文引用的文献

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Heart failure-induced cognitive dysfunction is mediated by intracellular Ca leak through ryanodine receptor type 2.心力衰竭引起的认知功能障碍是通过肌质网钙释放通道 2 介导的细胞内钙泄漏引起的。
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