日本一項最新研究稱，初步研究發現，用於治療暈車的藥物「美克洛嗪」有促進骨骼生長作用，但具體效果有待臨床檢驗。
日本名古屋大學醫學系副教授鬼頭浩史的研究涉及軟骨發育不全症。他和研究小組人員在美國在線科學雜誌《公共科學圖書館-綜合》上發表報告，稱如果基因FGFR3被異常激活，會導致軟骨發育不全症。如患這種疾病，成年後的身高僅有120至130釐米，還會出現椎管狹窄等症狀。這種疾病很難治療，目前一種方法是手術斷骨後再拉長，但會給患者身體帶來巨大負擔。
研究小組利用大鼠軟骨細胞測試多種藥物，結果發現美克洛嗪有遏制FGFR3的效果。研究小組還認為，除軟骨發育不全症，因體質原因導致個頭不高的人，如果能夠遏制FGFR3作用，也可能促進骨骼生長，增加身高。 （生物谷Bioon.com）
生物谷推薦的英文摘要
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.