中华地方病学杂志
中華地方病學雜誌
중화지방병학잡지
Chinese Journal of Endemiology
2014年
4期
367-369
,共3页
王慧敏%杜新爱%毋瑞朋%代晓霞%杜晓龙%刘继峰%白广禄%熊咏民
王慧敏%杜新愛%毌瑞朋%代曉霞%杜曉龍%劉繼峰%白廣祿%熊詠民
왕혜민%두신애%무서붕%대효하%두효룡%류계봉%백엄록%웅영민
大骨节病%磷脂酰肌醇3-激酶%蛋白激酶B%蛋白表达%信号转导
大骨節病%燐脂酰肌醇3-激酶%蛋白激酶B%蛋白錶達%信號轉導
대골절병%린지선기순3-격매%단백격매B%단백표체%신호전도
Kashin-Beck disease%Phosphatidylinositol 3-kinase%Protein kinase B%Protein expression%Signal transduction
目的：观察大骨节病患者全血中磷脂酰肌醇3-激酶（PI3K）及其下游蛋白激酶B（Akt）信号通路分子蛋白（PI3Kp110、pAkt、pGSK3β）表达，分析PI3K/Akt信号通路的状态。方法20例大骨节病患者（大骨节病组）来自陕西省大骨节病区（旬邑、麟游、永寿、千阳、长武、陇县），同时选取性别、年龄相匹配的健康者作为对照组。采集大骨节病患者和对照组人群静脉血，应用Trizol法从全血中提取蛋白，采用蛋白质免疫印迹试验（Western blot）检测全血中 PI3K/Akt 信号通路分子蛋白表达，十二烷基硫酸钠-聚丙烯酰胺凝胶电泳（SDS-PAGE），GDS-8000凝胶成像系统观察并记录灰度值，组间比较采用t检验。结果大骨节病组与对照组年龄、性别比较，差异无统计学意义（t=0.701，P>0.05；χ2=0.400，P>0.05）。大骨节病组全血中 PI3Kp110、pAkt、pGSK3β蛋白表达均明显高于对照组（156.1±92.1比79.5±21.5、113.7±15.2比43.3±10.7、105.9±17.5比37.3±12.0），两组比较差异有统计学意义（t=2.563、6.567、7.916，P<0.05或<0.01）。结论大骨节病患者全血中PI3K/Akt信号通路分子蛋白PI3Kp110、pAkt、pGSK3β表达明显增加，PI3K/Akt信号通路呈激活状态。
目的：觀察大骨節病患者全血中燐脂酰肌醇3-激酶（PI3K）及其下遊蛋白激酶B（Akt）信號通路分子蛋白（PI3Kp110、pAkt、pGSK3β）錶達，分析PI3K/Akt信號通路的狀態。方法20例大骨節病患者（大骨節病組）來自陝西省大骨節病區（旬邑、麟遊、永壽、韆暘、長武、隴縣），同時選取性彆、年齡相匹配的健康者作為對照組。採集大骨節病患者和對照組人群靜脈血，應用Trizol法從全血中提取蛋白，採用蛋白質免疫印跡試驗（Western blot）檢測全血中 PI3K/Akt 信號通路分子蛋白錶達，十二烷基硫痠鈉-聚丙烯酰胺凝膠電泳（SDS-PAGE），GDS-8000凝膠成像繫統觀察併記錄灰度值，組間比較採用t檢驗。結果大骨節病組與對照組年齡、性彆比較，差異無統計學意義（t=0.701，P>0.05；χ2=0.400，P>0.05）。大骨節病組全血中 PI3Kp110、pAkt、pGSK3β蛋白錶達均明顯高于對照組（156.1±92.1比79.5±21.5、113.7±15.2比43.3±10.7、105.9±17.5比37.3±12.0），兩組比較差異有統計學意義（t=2.563、6.567、7.916，P<0.05或<0.01）。結論大骨節病患者全血中PI3K/Akt信號通路分子蛋白PI3Kp110、pAkt、pGSK3β錶達明顯增加，PI3K/Akt信號通路呈激活狀態。
목적：관찰대골절병환자전혈중린지선기순3-격매（PI3K）급기하유단백격매B（Akt）신호통로분자단백（PI3Kp110、pAkt、pGSK3β）표체，분석PI3K/Akt신호통로적상태。방법20례대골절병환자（대골절병조）래자합서성대골절병구（순읍、린유、영수、천양、장무、롱현），동시선취성별、년령상필배적건강자작위대조조。채집대골절병환자화대조조인군정맥혈，응용Trizol법종전혈중제취단백，채용단백질면역인적시험（Western blot）검측전혈중 PI3K/Akt 신호통로분자단백표체，십이완기류산납-취병희선알응효전영（SDS-PAGE），GDS-8000응효성상계통관찰병기록회도치，조간비교채용t검험。결과대골절병조여대조조년령、성별비교，차이무통계학의의（t=0.701，P>0.05；χ2=0.400，P>0.05）。대골절병조전혈중 PI3Kp110、pAkt、pGSK3β단백표체균명현고우대조조（156.1±92.1비79.5±21.5、113.7±15.2비43.3±10.7、105.9±17.5비37.3±12.0），량조비교차이유통계학의의（t=2.563、6.567、7.916，P<0.05혹<0.01）。결론대골절병환자전혈중PI3K/Akt신호통로분자단백PI3Kp110、pAkt、pGSK3β표체명현증가，PI3K/Akt신호통로정격활상태。
Objective To observe the protein expressions of PI3Kp110, pAkt, pGSK3β of phosphatidylinositol 3-kinase (PI3K) and protein kinase B (Akt) signaling pathway in the whole blood of patients with Kashin-Beck disease and analyze the status of PI3K/Akt signaling pathway. Methods Patients with Kashin-Beck disease ( KBD group ) were from six counties ( Xunyi , Linyou , Yongshou , Qianyang , Changwu and Long County) of Shannxi Province in Kashin-Beck disease areas , and the healthy controls (control group) were matched by age and sex. Venous blood was collected from patients and healthy controls. Trizol method was applied to extract the whole blood protein; protein expression levels of PI3K/Akt signaling pathway in whole blood were detected by Western blotting; the gray values were observed and recorded by the sodium dodecyl sulfate polyacrylamide gel electrophoresis(SDS-PAGE) and GDS-8000 gel imaging analysis system. Differences between the two groups were assessed by Student’s t-test. Results Compared age and sex between KBD group and control group, differences were not statistically significant(t=0.701, P>0.05;χ2=0.400, P>0.05). The protein expression levels of PI3Kp110, pAkt and p-GSK3β in KBD group were higher than that in control group(156.1 ± 92.1 vs. 79.5 ± 21.5, 113.7 ± 15.2 vs. 43.3 ± 10.7 and 105.9 ± 17.5 vs. 37.3 ± 12.0, respectively) and the differences were statistically significant (t=2.563, 6.567, 7.916; all P < 0.05 or < 0.01). Conclusion The PI3Kp110, pAkt and p-GSK3β expressions of signaling pathway proteins in the whole blood of patiens with Kashin-Beck disease are up-regulated significantly and the status of PI3K/Akt signaling pathway is activated.
