中华老年医学杂志
中華老年醫學雜誌
중화노년의학잡지
Chinese Journal of Geriatrics
2013年
1期
58-60
,共3页
陈月云%王伟华%于智勇%王星
陳月雲%王偉華%于智勇%王星
진월운%왕위화%우지용%왕성
前列腺增生%热休克蛋白质类%肿瘤坏死因子-α%白细胞介素-1β
前列腺增生%熱休剋蛋白質類%腫瘤壞死因子-α%白細胞介素-1β
전렬선증생%열휴극단백질류%종류배사인자-α%백세포개소-1β
Prostatic hyperplasia%Heat-shock proteins%Tumor necrosis factor-alpha%Interleukins-1β
目的 探讨热休克蛋白70 (HSP70) mRNA、热休克蛋白22(HSP22) mRNA、肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)在老年良性前列腺增生(BPH)患者中的表达及意义,并观察非那雄胺的干预作用. 方法 选择住院合并BPH的老年患者68例及同期住院无BPH的老年患者30例.BPH患者随机分为常规治疗组(n=34)和非那雄胺组(n=34).应用逆转录聚合酶链反应(RT-PCR)方法检测所有入选者及BPH患者治疗后血清HSP70mRNA、HSP22mRNA,同时采用放射免疫分析法测定血清TNF-α、IL-1β的含量.根据国际前列腺症状评分量表(IPSS)评价BPH患者治疗前后前列腺增生症状改善情况. 结果 BPH患者HSP70mRNA、HSP22mRNA、TNF-α、IL-1β较无BPH患者明显增高(P＜0.01),治疗12周后非那雄胺治疗组HSP70mRNA、HSP22mRNA、TNF-α、IL-1β明显降低(P＜0.01,P＜0.05),常规治疗组较治疗前也有变化,但差异无统计学意义(P＞0.05).非那雄胺组治疗后HSP70mRNA、HSP22mRNA、TNF-α明显低于常规治疗组(P＜0.01,P＜0.05),而IL-1β与常规治疗组相比无明显差异(P＞0.05),IPSS积分也有明显改善(P＜0.05).IPSS积分与HSP70mRNA、HSP22mRNA、TNF-α、IL-1β表达呈正相关(r＝0.4251、0.4976、0.4562、0.3627,F＜0.01或P＜0.05). 结论 非那雄胺可能通过调节免疫炎性因子的表达抑制自身免疫性损伤从而改善BPH患者的症状.
目的 探討熱休剋蛋白70 (HSP70) mRNA、熱休剋蛋白22(HSP22) mRNA、腫瘤壞死因子-α(TNF-α)、白細胞介素-1β(IL-1β)在老年良性前列腺增生(BPH)患者中的錶達及意義,併觀察非那雄胺的榦預作用. 方法 選擇住院閤併BPH的老年患者68例及同期住院無BPH的老年患者30例.BPH患者隨機分為常規治療組(n=34)和非那雄胺組(n=34).應用逆轉錄聚閤酶鏈反應(RT-PCR)方法檢測所有入選者及BPH患者治療後血清HSP70mRNA、HSP22mRNA,同時採用放射免疫分析法測定血清TNF-α、IL-1β的含量.根據國際前列腺癥狀評分量錶(IPSS)評價BPH患者治療前後前列腺增生癥狀改善情況. 結果 BPH患者HSP70mRNA、HSP22mRNA、TNF-α、IL-1β較無BPH患者明顯增高(P＜0.01),治療12週後非那雄胺治療組HSP70mRNA、HSP22mRNA、TNF-α、IL-1β明顯降低(P＜0.01,P＜0.05),常規治療組較治療前也有變化,但差異無統計學意義(P＞0.05).非那雄胺組治療後HSP70mRNA、HSP22mRNA、TNF-α明顯低于常規治療組(P＜0.01,P＜0.05),而IL-1β與常規治療組相比無明顯差異(P＞0.05),IPSS積分也有明顯改善(P＜0.05).IPSS積分與HSP70mRNA、HSP22mRNA、TNF-α、IL-1β錶達呈正相關(r＝0.4251、0.4976、0.4562、0.3627,F＜0.01或P＜0.05). 結論 非那雄胺可能通過調節免疫炎性因子的錶達抑製自身免疫性損傷從而改善BPH患者的癥狀.
목적 탐토열휴극단백70 (HSP70) mRNA、열휴극단백22(HSP22) mRNA、종류배사인자-α(TNF-α)、백세포개소-1β(IL-1β)재노년량성전렬선증생(BPH)환자중적표체급의의,병관찰비나웅알적간예작용. 방법 선택주원합병BPH적노년환자68례급동기주원무BPH적노년환자30례.BPH환자수궤분위상규치료조(n=34)화비나웅알조(n=34).응용역전록취합매련반응(RT-PCR)방법검측소유입선자급BPH환자치료후혈청HSP70mRNA、HSP22mRNA,동시채용방사면역분석법측정혈청TNF-α、IL-1β적함량.근거국제전렬선증상평분량표(IPSS)평개BPH환자치료전후전렬선증생증상개선정황. 결과 BPH환자HSP70mRNA、HSP22mRNA、TNF-α、IL-1β교무BPH환자명현증고(P＜0.01),치료12주후비나웅알치료조HSP70mRNA、HSP22mRNA、TNF-α、IL-1β명현강저(P＜0.01,P＜0.05),상규치료조교치료전야유변화,단차이무통계학의의(P＞0.05).비나웅알조치료후HSP70mRNA、HSP22mRNA、TNF-α명현저우상규치료조(P＜0.01,P＜0.05),이IL-1β여상규치료조상비무명현차이(P＞0.05),IPSS적분야유명현개선(P＜0.05).IPSS적분여HSP70mRNA、HSP22mRNA、TNF-α、IL-1β표체정정상관(r＝0.4251、0.4976、0.4562、0.3627,F＜0.01혹P＜0.05). 결론 비나웅알가능통과조절면역염성인자적표체억제자신면역성손상종이개선BPH환자적증상.
Objective To explore the effects of finasteride therapy on the expressions of heat shock protein 70(HSP70)mRNA,heat shock protein 22 (HSP22)mRNA,tumor necrosis factor-alpha (TNF-a),interleukins-1β (IL-1β) in elderly patients with benign prostatic hyperplasia (BPH).Methods Totally 68 elderly men patients with BPH were divided into two groups:regular treatment group (n=34) and finasteride treatment group(n=34),30 elderly men patients without BPH were as control group.The blood samples of patients after treatment were collected for the detections of HSP70mRNA and HSP22mRNA with RT-PCR,meanwhile,the levels of TNF-α,IL-1β were measured by radioimmunoassay (RIA).Effect of treatment was evaluated in accordance with International Prostate Symptom Score (IPSS).Results The expressions of HSP70 mRNA and HSP22 mRNA,TNF-α,IL-1β in BPH patients were higher in finasteride group than in control group (P＜0.01).After 12 weeks therapy,the levels of HSP70mRNA,HSP22mRNA,TNF-α and IL-1β were decreased in finasteride group (P＜0.01 or P＜0.05) but no significantly difference in regular treatment group.Compared with regular treatment group,the expressions of HSP70 mRNA,HSP22mRNA and TNF-α were reduced in the finasteride group after treatment (P＜0.01 or P＜0.05),IPSS was more improved (P＜0.05),but IL-1β was not distingished between two groups (P＞0.05).IPSS was positively related to the levels of HSP70 mRNA,HSP22 mRNA,TNF-α and IL1β (r=0.4251,0.4976,0.4562,0.3627,P＜0.01 or P＜0.05).Conclusions The occurrence and development of BPH are closely related with immunoinflammatory factors.Finasteride not only affects the levels of dihydrotestosterone but also can inhibit the expression of immunoinflammatory factors to improve symptom by reducing the volume of benign prostatic hyperplasia.
