CAJ | 학술논문

目的：探讨正加速度对慢性胃溃疡大鼠血清生长素(ghrelin)及生长抑素(somatostatin，SS)的变化及作用机制。方法雄性SD大鼠24只，建立乙酸致大鼠慢性胃溃疡模型，造模后随机分为对照组、+5 Gz组和+10 Gz组，每组8只。3 d后模拟不同+Gz值正加速度条件，隔日1次，共4次，持续7 d。实验结束次日取大鼠胃黏膜及血液标本，HE染色病理切片，放射免疫法检测血清生长和生长抑素。结果在光镜下随+Gz值增高，胃黏膜腺体形态异常，排列紊乱，炎性细胞浸润明显。各+Gz值暴露组胃黏膜前列腺素E2(prostaglandin E2，PGE2)含量：+10 Gz组为3.438±0.908 pg/ml，+5 Gz组为5.147±0.652 pg/ml，对照组为6.986±0.743 pg/ml，+10 Gz组低于+5 Gz组(P＜0.05)，+5 Gz组低于对照组(P＜0.05)。各+Gz值暴露组血清生长素含量：+10 Gz组为(94.48±23.96) ng/ml，+5 Gz组为(142.56±38.63) ng/ml，对照组为(112.00±42.28) ng/ml，3组间差异有统计学意义(P＜0.05)，+10 Gz组明显低于对照组(P＜0.05)，+5 Gz组与对照组差异无统计学意义(P＞0.05)。各+Gz值暴露组血清SS含量：+10 Gz组(32.65±11.68) pg/ml，+5 Gz组为(51.52±10.88) pg/ml，对照组为(38.37±14.16) pg/ml，3组间差异有统计学意义(P＜0.05)，+5 Gz组明显高于对照组(P＜0.05)，+10 Gz组与对照组差异无统计学意义(P＞0.05)。结论随+Gz值增高，溃疡愈合质量下降；在中+Gz值条件下血清SS升高，在高+Gz值条件下血清生长素含量下降。
목적：탐토정가속도대만성위궤양대서혈청생장소(ghrelin)급생장억소(somatostatin，SS)적변화급작용궤제。방법웅성SD대서24지，건립을산치대서만성위궤양모형，조모후수궤분위대조조、+5 Gz조화+10 Gz조，매조8지。3 d후모의불동+Gz치정가속도조건，격일1차，공4차，지속7 d。실험결속차일취대서위점막급혈액표본，HE염색병리절편，방사면역법검측혈청생장화생장억소。결과재광경하수+Gz치증고，위점막선체형태이상，배렬문란，염성세포침윤명현。각+Gz치폭로조위점막전렬선소E2(prostaglandin E2，PGE2)함량：+10 Gz조위3.438±0.908 pg/ml，+5 Gz조위5.147±0.652 pg/ml，대조조위6.986±0.743 pg/ml，+10 Gz조저우+5 Gz조(P＜0.05)，+5 Gz조저우대조조(P＜0.05)。각+Gz치폭로조혈청생장소함량：+10 Gz조위(94.48±23.96) ng/ml，+5 Gz조위(142.56±38.63) ng/ml，대조조위(112.00±42.28) ng/ml，3조간차이유통계학의의(P＜0.05)，+10 Gz조명현저우대조조(P＜0.05)，+5 Gz조여대조조차이무통계학의의(P＞0.05)。각+Gz치폭로조혈청SS함량：+10 Gz조(32.65±11.68) pg/ml，+5 Gz조위(51.52±10.88) pg/ml，대조조위(38.37±14.16) pg/ml，3조간차이유통계학의의(P＜0.05)，+5 Gz조명현고우대조조(P＜0.05)，+10 Gz조여대조조차이무통계학의의(P＞0.05)。결론수+Gz치증고，궤양유합질량하강；재중+Gz치조건하혈청SS승고，재고+Gz치조건하혈청생장소함량하강。
Objective To study the serum ghrelin and somatostatin (SS) level in rats with experimental gastric ulcer under positive acceleration and its mechanism. Methods A rat chronic gastric ulcer model was induced by acetic acid. Twenty-four male SD rats with gastric ulcer were randomly divided into control group,+5 Gz group, and+10 Gz group (8 in each group). The rats were treated 4 times by simulating positive acceleration every other day for 1 week 3 days after experiment. Gastric mucosa tissue and blood samples were taken on the next day after experiment. Pathological sections were stained with H&E. Serum ghrelin and SS levels were measured by RIA. Results Optical microscopy showed abnormal morphology of disordered gastric mucosal glands with obvious infiltration of inflammatory cells when the+Gz was higher. The serum PGE2 level in gastric mucosa was 3.438±0.908 pg/ml in+10 Gz group, 5.147±0.652 pg/ml in+5 Gz group and 6.986±0.743 pg/ml in control group (P < 0.05). The serum ghrelin level was 94.48±23.96 ng/ml in+10 Gz group, 142.56±38.63 ng/ml in+5 Gz group and 112.00±42.28 ng/ml in control group (P<0.05). The serum SS level was 32.65±11.68 pg/ml in +10 Gz group, 51.52±10.88 pg/ml in +5 Gz group and 38.37±14.16 pg/ml in control group (P<0.05). Conclusion The ulcer healing is poor when the+Gz increases. The serum SS level increases when the+Gz maintains at a moderate level whereas the serum ghrelin level decreases when the+Gz maintains at a high level.