Allanson Munif, Reeve Vivienne E
Faculty of Veterinary Science, University of Sydney, Sydney, NSW, Australia.
Cancer Immunol Immunother. 2007 Nov;56(11):1807-15. doi: 10.1007/s00262-007-0324-1. Epub 2007 Apr 18.
Exposure of the skin of mice to UVA (320-400 nm) radiation has been shown to provide protection against the immunosuppressive effects of UVB (290-320 nm) radiation. The UVA protection was mediated via the UVA induction of the stress protein heme oxygenase-1, and its enzymatic product carbon monoxide (CO). Because UVB-induced immunosuppression is an accompanying and prerequisite feature of the promotion phase of photocarcinogenesis, the potential for immunoprotective CO to act as an anti-skin cancer agent was tested in this study. Groups of female albino Skh:hr-1 hairless mice were irradiated chronically with daily minimally erythemogenic doses of solar simulated UV radiation (SSUV) during a 10 week-period to induce photocarcinogenesis. The effect of repeated topical application of lotions containing a CO-releasing molecule (CORM-2; tricarbonyldichlororuthenium (II) dimer) at 250 or 500 microM, that had previously been shown in short-term experiments to provide photoimmune protection in mice, was measured. Tumor development was monitored for 29 weeks. Topical CORM-2 treatment was observed to reduce the acute and chronic inflammatory erythema reaction compared with control irradiated mice that did not receive CORM-2 lotions, and to reduce the chronic epidermal hyperplasia accompanying tumor outgrowth. The CORM-2 treatments provided a significant moderate inhibition of early tumor appearance dose-dependently, significantly reduced the average tumor multiplicity, increased the regression of established tumors dose-dependently, and inhibited the formation of large locally invasive tumors. The CORM-2 treatments also reduced the expression of immunosuppressive IL-10 in the uninvolved epidermis and dermis of tumor-bearing mice, and enhanced immunopotentiating epidermal IL-12 expression. Therefore CO signalling was revealed to have previously unrecognized anti-carcinogenic functions in the skin, consistent with a protective modulation of the epidermal cytokines. This is a novel observation that also implies that the UVA waveband that produces CO physiologically in exposed skin, might likewise be found to have an anti-photocarcinogenic action.
已证明,将小鼠皮肤暴露于UVA(320 - 400纳米)辐射下,可提供针对UVB(290 - 320纳米)辐射免疫抑制作用的保护。UVA保护作用是通过应激蛋白血红素加氧酶-1及其酶促产物一氧化碳(CO)的UVA诱导介导的。由于UVB诱导的免疫抑制是光致癌促进阶段的伴随特征和先决条件,本研究测试了具有免疫保护作用的CO作为抗皮肤癌药物的潜力。将雌性白化病Skh:hr-1无毛小鼠分组,在10周期间每天用最低红斑剂量的太阳模拟紫外线辐射(SSUV)进行慢性照射,以诱导光致癌作用。测量了重复局部应用含250或500微摩尔一氧化碳释放分子(CORM-2;二氯羰基钌(II)二聚体)的洗剂的效果,此前在短期实验中已证明该洗剂可在小鼠中提供光免疫保护。对肿瘤发展进行了29周的监测。与未接受CORM-2洗剂的对照照射小鼠相比,观察到局部应用CORM-2治疗可减少急性和慢性炎症性红斑反应,并减少伴随肿瘤生长的慢性表皮增生。CORM-2治疗剂量依赖性地对早期肿瘤出现提供了显著的中度抑制,显著降低了平均肿瘤多发性,剂量依赖性地增加了已形成肿瘤的消退,并抑制了大的局部侵袭性肿瘤的形成。CORM-2治疗还降低了荷瘤小鼠未受累表皮和真皮中免疫抑制性IL-10的表达,并增强了免疫增强性表皮IL-12的表达。因此,揭示了CO信号在皮肤中具有以前未被认识的抗癌功能,这与表皮细胞因子的保护性调节一致。这是一项新的观察结果,也意味着在暴露皮肤中生理产生CO的UVA波段可能同样具有抗光致癌作用。