CAJ | 학술논문

　　目的：检测寻常型银屑病(PV)患者皮损及外周血单一核细胞(PBMC)中血红素氧合酶-1(HO-1)mRNA和蛋白的表达。方法：逆转录-聚合酶链反应(RT-PCR)法和免疫组化方法检测20例PV患者和10例正常人皮肤及PBMC中HO-1 mRNA 和蛋白的表达。结果： PV患者及正常对照组皮肤中HO-1mRNA表达相对含量分别为1.32±0.29和0.46±0.10，HO-1的免疫组化评分分别为10.25±2.36和2.65±1.03；患者及对照组PBMC中HO-1mRNA相对含量分别为0.25±0.14和0.22±0.16，HO-1染色阳性细胞的百分比为11.7％±3.44％和10.5％±4.06％，PV皮损中HO-1的mRNA和蛋白表达明显高于正常对照组(P<0.05)，而PV患者外周血PBMC中HO-1 mRNA和蛋白的表达水平与正常对照组差异无显著性(P>0.05)。结论： HO-1可能参与了银屑病皮损的发病过程。
　　목적：검측심상형은설병(PV)환자피손급외주혈단일핵세포(PBMC)중혈홍소양합매-1(HO-1)mRNA화단백적표체。방법：역전록-취합매련반응(RT-PCR)법화면역조화방법검측20례PV환자화10례정상인피부급PBMC중HO-1 mRNA 화단백적표체。결과： PV환자급정상대조조피부중HO-1mRNA표체상대함량분별위1.32±0.29화0.46±0.10，HO-1적면역조화평분분별위10.25±2.36화2.65±1.03；환자급대조조PBMC중HO-1mRNA상대함량분별위0.25±0.14화0.22±0.16，HO-1염색양성세포적백분비위11.7％±3.44％화10.5％±4.06％，PV피손중HO-1적mRNA화단백표체명현고우정상대조조(P<0.05)，이PV환자외주혈PBMC중HO-1 mRNA화단백적표체수평여정상대조조차이무현저성(P>0.05)。결론： HO-1가능삼여료은설병피손적발병과정。
Objective:To detect the expression level of heme oxygenase-1 (HO-1) mRNA and protein in skin lesions and peripheral blood mononuclear cell (PBMC) of the patients with psoriasis vulgaris ( PV). Methods:RT-PCR and immunohistochemical staining were applied to determine the expression of HO-1mRNA and protein in skin lesions and PBMC from 20 PV patients and 10 normal controls. Results:The lev￣els of HO-1 mRNA in skin lesions of patients with PV and normal controls were (1.32±0.29) and (0.46± 0.10) respectively,the immunohistochemical score of HO-1 protein were (10.25±2.36)and (2.65±1.03) re￣spectively. The levels of HO-1 mRNA in PBMC of patients and normal controls were (0.25±0.14) and (0.22 ±0.16) respectively. The positivity of immunohistochemical staining of HO-1 protein in the patients and con￣trols were (11.7±3.44)% and (10.5±4.06)% respectively. The content of HO-1mRNA and the expression level of HO-1 protein in skin lesions of patients with PV was obviously higher than those in controls (P<0.05). However,there was no significant difference in the content of HO-1 mRNA and the expression level of HO-1 protein in PBMC between the two groups (P>0.05). Conclusion:HO-1 may be involved in the patho￣genesis of PV.