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PLoS ONE:晕车药或有助长高

  1. 晕车药
  2. 有助
  3. 长高

来源:新华社 2013-12-09 13:18

日本一项最新研究称,初步研究发现,用于治疗晕车的药物“美克洛嗪”有促进骨骼生长作用,但具体效果有待临床检验。

日本一项最新研究称,初步研究发现,用于治疗晕车的药物“美克洛嗪”有促进骨骼生长作用,但具体效果有待临床检验。

日本名古屋大学医学系副教授鬼头浩史的研究涉及软骨发育不全症。他和研究小组人员在美国在线科学杂志《公共科学图书馆-综合》上发表报告,称如果基因FGFR3被异常激活,会导致软骨发育不全症。如患这种疾病,成年后的身高仅有120至130厘米,还会出现椎管狭窄等症状。这种疾病很难治疗,目前一种方法是手术断骨后再拉长,但会给患者身体带来巨大负担。

研究小组利用大鼠软骨细胞测试多种药物,结果发现美克洛嗪有遏制FGFR3的效果。研究小组还认为,除软骨发育不全症,因体质原因导致个头不高的人,如果能够遏制FGFR3作用,也可能促进骨骼生长,增加身高。 (生物谷Bioon.com)

生物谷推荐的英文摘要

PLoS ONE                 DOI: 10.1371/journal.pone.0081569

Meclozine Facilitates Proliferation and Differentiation of Chondrocytes by Attenuating Abnormally Activated FGFR3 Signaling in Achondroplasia

Masaki Matsushita, Hiroshi Kitoh, Bisei Ohkawara, Kenichi Mishima, Hiroshi Kaneko, Mikako Ito, Akio Masuda, Naoki Ishiguro, Kinji Ohno

Achondroplasia (ACH) is one of the most common skeletal dysplasias with short stature caused by gain-of-function mutations in FGFR3 encoding the fibroblast growth factor receptor 3. We used the drug repositioning strategy to identify an FDA-approved drug that suppresses abnormally activated FGFR3 signaling in ACH. We found that meclozine, an anti-histamine drug that has long been used for motion sickness, facilitates chondrocyte proliferation and mitigates loss of extracellular matrix in FGF2-treated rat chondrosarcoma (RCS) cells. Meclozine also ameliorated abnormally suppressed proliferation of human chondrosarcoma (HCS-2/8) cells that were infected with lentivirus expressing constitutively active mutants of FGFR3-K650E causing thanatophoric dysplasia, FGFR3-K650M causing SADDAN, and FGFR3-G380R causing ACH. Similarly, meclozine alleviated abnormally suppressed differentiation of ATDC5 chondrogenic cells expressing FGFR3-K650E and -G380R in micromass culture. We also confirmed that meclozine alleviates FGF2-mediated longitudinal growth inhibition of embryonic tibia in bone explant culture. Interestingly, meclozine enhanced growth of embryonic tibia in explant culture even in the absence of FGF2 treatment. Analyses of intracellular FGFR3 signaling disclosed that meclozine downregulates phosphorylation of ERK but not of MEK in FGF2-treated RCS cells. Similarly, meclozine enhanced proliferation of RCS cells expressing constitutively active mutants of MEK and RAF but not of ERK, which suggests that meclozine downregulates the FGFR3 signaling by possibly attenuating ERK phosphorylation. We used the C-natriuretic peptide (CNP) as a potent inhibitor of the FGFR3 signaling throughout our experiments, and found that meclozine was as efficient as CNP in attenuating the abnormal FGFR3 signaling. We propose that meclozine is a potential therapeutic agent for treating ACH and other FGFR3-related skeletal dysplasias.

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