中华皮肤科杂志
中華皮膚科雜誌
중화피부과잡지
Chinese Journal of Dermatology
2014年
10期
719-722
,共4页
胡小平%张伟%陈办成%陈史宏%王勇强%于波
鬍小平%張偉%陳辦成%陳史宏%王勇彊%于波
호소평%장위%진판성%진사굉%왕용강%우파
银屑病%角蛋白细胞%过氧化物酶体增生物激活受体β/δ
銀屑病%角蛋白細胞%過氧化物酶體增生物激活受體β/δ
은설병%각단백세포%과양화물매체증생물격활수체β/δ
Psoriasis%Keratinocytes%PPARβ/δ
目的 探讨过氧化物酶增殖物激活受体β/δ (PPARβ/δ)在银屑病患者表皮角质形成细胞(KC)中的表达和调节因素.方法 免疫组化方法检测PPARβ/δ在银屑病患者皮损及非皮损表皮中的表达.分离、培养银屑病患者非皮损区和皮损区的KC,以RT-PCR和Western印迹法分别检测银屑病患者皮损区和非皮损区KC中PPARβ/δ mRNA和蛋白质的表达水平.利用PPARβ/δ外源性激动剂GW501516及Ca2+刺激银屑病非皮损区KC,观察其对PPARβ/δ表达的调节影响.结果 免疫组化显示,银屑病皮损区PPARβ/δ的表达强度显著高于正常对照组(t=19.28,P<0.01)和非皮损区(t=23.26,P<0.01).银屑病皮损区PPARβ/δ mRNA和蛋白质的表达水平均高于正常对照组(P<0.01)和非皮损区(P< 0.01).10 ng/ml GW501516最大效能促进PPARβ/δ的表达(P< 0.01);1.0 mmol/L Ca2+对KC中PPARβ/δ的表达促进效应最明显(P<0.01).结论 PPARβ/δ在银屑病患者皮损区表达显著升高,GW501516和CaCa2+能够促进角质形成细胞PPARβ/δ表达水平.
目的 探討過氧化物酶增殖物激活受體β/δ (PPARβ/δ)在銀屑病患者錶皮角質形成細胞(KC)中的錶達和調節因素.方法 免疫組化方法檢測PPARβ/δ在銀屑病患者皮損及非皮損錶皮中的錶達.分離、培養銀屑病患者非皮損區和皮損區的KC,以RT-PCR和Western印跡法分彆檢測銀屑病患者皮損區和非皮損區KC中PPARβ/δ mRNA和蛋白質的錶達水平.利用PPARβ/δ外源性激動劑GW501516及Ca2+刺激銀屑病非皮損區KC,觀察其對PPARβ/δ錶達的調節影響.結果 免疫組化顯示,銀屑病皮損區PPARβ/δ的錶達彊度顯著高于正常對照組(t=19.28,P<0.01)和非皮損區(t=23.26,P<0.01).銀屑病皮損區PPARβ/δ mRNA和蛋白質的錶達水平均高于正常對照組(P<0.01)和非皮損區(P< 0.01).10 ng/ml GW501516最大效能促進PPARβ/δ的錶達(P< 0.01);1.0 mmol/L Ca2+對KC中PPARβ/δ的錶達促進效應最明顯(P<0.01).結論 PPARβ/δ在銀屑病患者皮損區錶達顯著升高,GW501516和CaCa2+能夠促進角質形成細胞PPARβ/δ錶達水平.
목적 탐토과양화물매증식물격활수체β/δ (PPARβ/δ)재은설병환자표피각질형성세포(KC)중적표체화조절인소.방법 면역조화방법검측PPARβ/δ재은설병환자피손급비피손표피중적표체.분리、배양은설병환자비피손구화피손구적KC,이RT-PCR화Western인적법분별검측은설병환자피손구화비피손구KC중PPARβ/δ mRNA화단백질적표체수평.이용PPARβ/δ외원성격동제GW501516급Ca2+자격은설병비피손구KC,관찰기대PPARβ/δ표체적조절영향.결과 면역조화현시,은설병피손구PPARβ/δ적표체강도현저고우정상대조조(t=19.28,P<0.01)화비피손구(t=23.26,P<0.01).은설병피손구PPARβ/δ mRNA화단백질적표체수평균고우정상대조조(P<0.01)화비피손구(P< 0.01).10 ng/ml GW501516최대효능촉진PPARβ/δ적표체(P< 0.01);1.0 mmol/L Ca2+대KC중PPARβ/δ적표체촉진효응최명현(P<0.01).결론 PPARβ/δ재은설병환자피손구표체현저승고,GW501516화CaCa2+능구촉진각질형성세포PPARβ/δ표체수평.
Objective To measure the expression of peroxisome proliferator-activated receptor β/δ (PPARβ/δ) in epidermal keratinocytes from patients with psoriasis,and to investigate its regulatory factors.Methods Tissue specimens were obtained from both lesional and non-lesional skin of 20 patients with psoriasis as well as from normal skin of 15 human controls.An immunohistochemical method was used to examine the expression of PPARβ/δ in these tissue specimens.Epidermal keratinocytes were isolated from these tissue specimens and subjected to a primary culture.After several passages of subculture,non-lesional psoriatic keratinocytes were stimulated with different concentrations of GW501516 (an agonist of PPARβ/δ,0-100 ng/ml) and Ca2+ (0-3.0 mmol/L).Reverse transcription-PCR and Western blot were performed to measure the mRNA and protein expressions of PPARβ/δ in the primary keratinocytes and stimulated keratinocytes respectively.Results Immunohistochemistry showed that the expression intensity of PPARβ/δ was significantly higher in lesional psoriatic skin than in normal control skin (t =19.28,P < 0.01) and non-lesional psoriatic skin (t =23.26,P < 0.01).Increased mRNA and protein levels of PPARβ/δ were observed in lesional psoriatic keratinocytes as compared to normal control keratinocytes (both P <0.01) and non-lesional psoriatic keratinocytes (both P < 0.01).Among these stimulated non-lesional psoriatic keratinocytes,those treated with GW501516 at 10 ng/ml and those with Ca2+ of 1.0 mmol/L showed the strongest expression of PPARβ/δ (both P < 0.01).Conclusions The expression of PPARβ/δ,which is higher in lesional psoriatic skin,can be enhanced by GW501516 and Ca2+ in keratinocytes.