Ye Juan, Lee Sang Yeul, Kook Koung Hoon, Yao Ke
Department of Ophthalmology, The 2nd Affiliated Hospital of Zhejiang University, College of Medicine, Hangzhou, Zhejiang, China.
Graefes Arch Clin Exp Ophthalmol. 2008 Feb;246(2):217-22. doi: 10.1007/s00417-007-0716-0. Epub 2007 Dec 11.
To determine whether bone marrow-derived progenitor cells can be stimulated by inflammatory mediators and play a role in corneal wound healing following alkali injury.
Sixty rabbits were divided into two groups (Group I and Group II). Group I served as a bone marrow-suppression model, and received 200 mg/kg cyclophosphamide. Corneal alkali injury was created in one eye of each rabbit in each group; the other eye served as control. Three days after corneal burn, inflammatory cells in peripheral blood were counted. At the end of 4 weeks follow-up, corneas of all rabbits were subjected to histochemical examination to assess infiltrated CD34 and C-kit positive cells. Clinical outcome was determined at the end of 4 weeks.
Cyclophosphamide suppressed bone marrow function in Group I by reducing cellularity by more than 30% and neutrophil distribution by 3.18 +/- 1.83%. The number of bone marrow hematopoietic and mesenchymal progenitor cells were all suppressed by cyclophophamide, as demonstrated by statistically significant differences between Group I and Group II of CD34+ cells (t = -21.62, P < 0.01) and C-Kit cells (t = -21.62, P < 0.01). Fewer inflammatory cells were released into circulation in Group I (14.42 +/- 5.70%) than in Group II (44.36 +/- 8.64%). Clinical observation revealed that Group II rabbits had much greater reepithelization (t = 6.999, P < 0.01) and clearer corneas (X(2) = 4.417, P < 0.01) than Group I.
Corneal alkali injury is a stimulus that induces a rapid bone marrow reaction to release not only inflammatory cells but also progenitor cells into circulation. Migrated bone marrow-derived progenitor cells can home to local sites to promote wound healing.
确定骨髓来源的祖细胞是否能被炎症介质刺激，并在碱烧伤后的角膜伤口愈合中发挥作用。
60只兔子分为两组（I组和II组）。I组作为骨髓抑制模型，接受200mg/kg环磷酰胺。每组每只兔子的一只眼睛造成角膜碱烧伤；另一只眼睛作为对照。角膜烧伤3天后，计数外周血中的炎症细胞。在4周随访结束时，对所有兔子的角膜进行组织化学检查，以评估浸润的CD34和C-kit阳性细胞。在4周结束时确定临床结果。
环磷酰胺通过使细胞数量减少超过30%和中性粒细胞分布减少3.18±1.83%来抑制I组的骨髓功能。环磷酰胺抑制了骨髓造血祖细胞和间充质祖细胞的数量，I组和II组CD34+细胞（t=-21.62，P<0.01）和C-Kit细胞（t=-21.62，P<0.01）之间的统计学显著差异证明了这一点。I组释放到循环中的炎症细胞（14.42±5.70%）比II组（44.36±8.64%）少。临床观察显示，II组兔子的角膜再上皮化程度（t=6.999，P<0.01）和角膜清晰度（X(2)=4.417，P<0.01）均明显高于I组。
角膜碱烧伤是一种刺激因素，可诱导骨髓快速反应，不仅将炎症细胞而且将祖细胞释放到循环中。迁移的骨髓来源祖细胞可归巢至局部部位以促进伤口愈合。
