Department of Physiology, School of Basic Medical Science Central South University, Changsha, China.
Peptides. 2013 Feb;40:34-41. doi: 10.1016/j.peptides.2012.11.017. Epub 2012 Dec 5.
Epidemiological data indicate an increasing incidence of asthma in the obese individuals recent decades, while very little is known about the possible association between them. Here, we compared the roles of adipocyte-derived factors, including leptin, adiponectin and resistin on proliferation, wound repair and apoptosis in human bronchial epithelial cells (HBECs) which play an important role in the pathogenesis of asthma. The results showed that exogenous globular adiponectin (gAd) promoted proliferation, cell-cycle and wound repair of HBECs. This effect may be relevant to Ca(2+)/calmodulin signal pathway. Besides, gAd inhibited apoptosis induced by ozone and release of lactate dehydrogenase (LDH) of HBECs via regulated adipoR1 and reactive oxygen species. No effects of leptin or resistin on proliferation, wound repair and apoptosis of HBECs were detectable. These data indicate that airway epithelium is the direct target of gAd which plays an important role in protecting HBECs from mechanical or oxidant injuries and may have therapeutic implications in the treatment of asthma.
流行病学数据表明，近几十年来肥胖人群中哮喘的发病率不断上升，而对于它们之间可能存在的关联却知之甚少。在这里，我们比较了脂肪细胞衍生因子（包括瘦素、脂联素和抵抗素）在人支气管上皮细胞（HBEC）增殖、伤口修复和细胞凋亡中的作用，这些因子在哮喘发病机制中起着重要作用。结果表明，外源性球状脂联素（gAd）促进了 HBEC 的增殖、细胞周期和伤口修复。这种作用可能与 Ca（2+）/钙调蛋白信号通路有关。此外，gAd 通过调节 adipoR1 和活性氧来抑制臭氧诱导的 HBEC 凋亡和乳酸脱氢酶（LDH）的释放。瘦素或抵抗素对 HBEC 的增殖、伤口修复和凋亡没有影响。这些数据表明，气道上皮细胞是 gAd 的直接靶标，它在保护 HBEC 免受机械或氧化损伤方面起着重要作用，这可能对哮喘的治疗具有治疗意义。
