CAJ | 학술논문

目的：探讨垂体瘤转化基因(PTTG)在垂体细胞衰老和垂体瘤中表达规律。方法构建F344大鼠D-半乳糖诱导衰老模型和雌激素诱导泌乳素腺瘤模型。观察大鼠的衰老表型及成瘤情况，对大鼠垂体进行病理学检测，分子生物学方法检测垂体PTTG、P53、P21、P16蛋白表达。结果①D-半乳糖成功诱导大鼠出现明显衰老特征，雌激素诱导大鼠成功生成泌乳素腺瘤；②衰老大鼠垂体胞质内有空泡和异染色质生成，肿瘤大鼠垂体PRL免疫组化为强阳性；③RT-PCR显示雌激素诱导组PTTG mRNA表达为(12.99±1.86)，D-半乳糖诱导衰老组PTTG表达为(2.10±0.23)，差异有高度统计学意义(P<0.01)；D-半乳糖诱导衰老组P53、P16、P21 mRNA表达为(113.51±23.87)、(29.26±4.44)、(67.21±10.08)，在雌激素诱导垂体瘤组中表达为(83.26±8.06)、(9.83±2.13)、(28.19±2.01)，两组比较差异有统计学意义(P<0.05)。④Western-blot条带积分灰度值显示D-半乳糖诱导衰老组PTTG、P21、P16蛋白表达为(0.198±0.032)、(1.239±0.051)、(1.673±0.055)，雌激素诱导垂体瘤中表达为(1.002±0.041)、(0.202±0.055)、(0.409±0.059)，两组比较差异有统计学意义(P<0.05)。结论 PTTG基因过表达导致衰老绕过，垂体瘤形成。 PTTG表达减弱，诱导衰老。 P16、P21是垂体细胞衰老重要的调控因子。
목적：탐토수체류전화기인(PTTG)재수체세포쇠로화수체류중표체규률。방법구건F344대서D-반유당유도쇠로모형화자격소유도비유소선류모형。관찰대서적쇠로표형급성류정황，대대서수체진행병이학검측，분자생물학방법검측수체PTTG、P53、P21、P16단백표체。결과①D-반유당성공유도대서출현명현쇠로특정，자격소유도대서성공생성비유소선류；②쇠로대서수체포질내유공포화이염색질생성，종류대서수체PRL면역조화위강양성；③RT-PCR현시자격소유도조PTTG mRNA표체위(12.99±1.86)，D-반유당유도쇠로조PTTG표체위(2.10±0.23)，차이유고도통계학의의(P<0.01)；D-반유당유도쇠로조P53、P16、P21 mRNA표체위(113.51±23.87)、(29.26±4.44)、(67.21±10.08)，재자격소유도수체류조중표체위(83.26±8.06)、(9.83±2.13)、(28.19±2.01)，량조비교차이유통계학의의(P<0.05)。④Western-blot조대적분회도치현시D-반유당유도쇠로조PTTG、P21、P16단백표체위(0.198±0.032)、(1.239±0.051)、(1.673±0.055)，자격소유도수체류중표체위(1.002±0.041)、(0.202±0.055)、(0.409±0.059)，량조비교차이유통계학의의(P<0.05)。결론 PTTG기인과표체도치쇠로요과，수체류형성。 PTTG표체감약，유도쇠로。 P16、P21시수체세포쇠로중요적조공인자。
Objective To investigate the pituitary tumor transforming gene (PTTG) expression pattern in pituitary cell senescence and pituitary adenoma tumorigenesis. Methods D-galactose induced F344 rats aging model. The rats aging expression and tumor generation condition were observed through pathological detection, molecular biology method was used to measure the expression of PTTG, P53, P21, P16 in pituitary tissue. Results ①D-galactose induced F344 rats showed significant characteristics of aging and oestrogen induced rats successfully generated prolactin adenoma; ②ag-ing Rats visible cytoplasmic vacuoles occurred, heterochromatin exists in the pituitary cell, pituitary PRL immunohisto-chemical was strong positive in tumor group rats; ③RT-PCR showed that PTTG mRNA expression in estrogen induced pituitary adenoma group was (12.99±1.86), PTTG expression of D-galactose induced aging group was (2.10±0.23), the difference was statistically significant (P<0.01); P53, P16, P21 mRNA expression of D-galactose induced aging group was (113.51±23.87), (29.26±4.44), (67.21±10.08), P53, P16, P21 mRNA expressed in estrogen induction of pituitary adenoma group was (83.26±8.06), (9.83±2.13), (28.19±2.01), the differences were statistically significant (P< 0.05); ④Western-blot strip integral grey value showed PTTG, P21 and P16 protein expression of D-galactose induced aging group was (0.198±0.032), (1.239±0.051), (1.673±0.055) and expressed in estrogen induced pituitary adenoma group was (1.002±0.041), (0.202±0.055), (0.409±0.059), the differences were statistically significant (P<0.05). Conclusion PTTG over-expression leads to senescence bypassed pituitary adenoma formation, PTTG weak expression leads to senescence. P16, P21 are important regulatory factors in pituitary cell senescence.