中华胰腺病杂志
中華胰腺病雜誌
중화이선병잡지
CHINESE JOURNAL OF PANCREATOLOGY
2011年
4期
278-280
,共3页
李嘉%刘爽%孙海晨%崔叶青%李非
李嘉%劉爽%孫海晨%崔葉青%李非
리가%류상%손해신%최협청%리비
胰腺%纤维化%结缔组织生长因子%星形细胞
胰腺%纖維化%結締組織生長因子%星形細胞
이선%섬유화%결체조직생장인자%성형세포
Pancreatic%Fibrosis%Connective tissue growth factor%Astrocytes
目的 观察胰腺纤维化后结缔组织生长因子(connective tissue growth factor,CTGF)在胰腺组织内的表达,探讨其意义。方法 通过高脂饲料诱导大鼠胰腺纤维化模型,16周后处死大鼠,取胰腺组织常规病理检查,天狼猩红染色和免疫组织化学染色检测胰腺纤维化组织胶原蛋白I、α-SMA及CTGF蛋白表达。结果 胰腺纤维化后,胰腺小叶和腺泡萎缩,小叶间隙增宽,间质内纤维组织明显增生;胰腺组织内胶原蛋白Ⅰ的合成较正常胰腺明显增加(1207.3±115.5比166.7±78.4,P<0.01),α-SMA 表达量较正常胰腺组织增高(1500.2±255.8比57.4±23.2,P<0.01),CTGF表达较正常胰腺明显增加(2950.5±431.9比382.2±190.8,P<0.01),且胰腺星状细胞(PSCs)大量活化。结论 CTGF是胰腺纤维化的重要作用因子,其作用与PSCs活化密切相关。
目的 觀察胰腺纖維化後結締組織生長因子(connective tissue growth factor,CTGF)在胰腺組織內的錶達,探討其意義。方法 通過高脂飼料誘導大鼠胰腺纖維化模型,16週後處死大鼠,取胰腺組織常規病理檢查,天狼猩紅染色和免疫組織化學染色檢測胰腺纖維化組織膠原蛋白I、α-SMA及CTGF蛋白錶達。結果 胰腺纖維化後,胰腺小葉和腺泡萎縮,小葉間隙增寬,間質內纖維組織明顯增生;胰腺組織內膠原蛋白Ⅰ的閤成較正常胰腺明顯增加(1207.3±115.5比166.7±78.4,P<0.01),α-SMA 錶達量較正常胰腺組織增高(1500.2±255.8比57.4±23.2,P<0.01),CTGF錶達較正常胰腺明顯增加(2950.5±431.9比382.2±190.8,P<0.01),且胰腺星狀細胞(PSCs)大量活化。結論 CTGF是胰腺纖維化的重要作用因子,其作用與PSCs活化密切相關。
목적 관찰이선섬유화후결체조직생장인자(connective tissue growth factor,CTGF)재이선조직내적표체,탐토기의의。방법 통과고지사료유도대서이선섬유화모형,16주후처사대서,취이선조직상규병리검사,천랑성홍염색화면역조직화학염색검측이선섬유화조직효원단백I、α-SMA급CTGF단백표체。결과 이선섬유화후,이선소협화선포위축,소협간극증관,간질내섬유조직명현증생;이선조직내효원단백Ⅰ적합성교정상이선명현증가(1207.3±115.5비166.7±78.4,P<0.01),α-SMA 표체량교정상이선조직증고(1500.2±255.8비57.4±23.2,P<0.01),CTGF표체교정상이선명현증가(2950.5±431.9비382.2±190.8,P<0.01),차이선성상세포(PSCs)대량활화。결론 CTGF시이선섬유화적중요작용인자,기작용여PSCs활화밀절상관。
Objective To observe the expression of connective tissue growth factor (CTGF) in pancreas, and discuss its significance. Methods The pancreatic fibrosis model was induced by high fat diets. The rats were sacrificed 16 weeks later, and the pancreatic tissue was harvested for routine pathologic examinations. Pancreatic collagen fibrosis I was determined by HE and Sirius red staining;α-SMA and CTGF expression were detected by immunohistochemistry. Results After pancreatic fibrosis, pancreatic lobules and acinar atrophy was observed, lobules gap was widened, interstitial fibrous tissue was significantly proliferated, the synthesis of pancreatic collagen fibrosis I was significantly increased when compared with normal pancreas ( 1500.2 + 255.8 vs. 57.4 ± 23.2, P < 0. 01 ), the expression of α-SMA was significantly increased when compared with normal pancreas( 1500.2 + 255.8 vs. 57.4 + 23.2, P < 0. 01 ), and the expression of CTGF was significantly increased when compared with normal pancreas (2950.5 ± 431.9 vs. 382.2 + 190.8, P <0.01 ), and there were abundant activated PSCs. Conclusions CTGF participated in the regulation of pancreatic fibrosis development; the function of CTGF was closely related to PSCs activation.