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大鼠实验性结肠炎中丁酸盐、美沙拉嗪和凝血因子 XIII:对转谷氨酰胺酶活性的影响

Butyrate, mesalamine, and factor XIII in experimental colitis in the rat: effects on transglutaminase activity.

作者信息

D'Argenio G, Cosenza V, Sorrentini I, De Ritis F, Gatto A, Delle Cave M, D'Armiento F P, Mazzacca G

机构信息

Department of Gastroenterology, School of Medicine, Federico II University, Naples, Italy.

出版信息

Gastroenterology. 1994 Feb;106(2):399-404. doi: 10.1016/0016-5085(94)90598-3.

DOI:10.1016/0016-5085(94)90598-3
PMID:7905450
Abstract

BACKGROUND/AIMS: Butyrate and factor XIII may improve ulcerative colitis; they also affect tissue and serum transglutaminase levels. We investigated the therapeutic potential of sodium butyrate and factor XIII and the role of transglutaminase during mucosal repair in experimental colitis.

METHODS

Rats with induced colitis were treated with sodium butyrate, mesalamine, sodium butyrate plus mesalamine, or saline enemas. Thromboxane B2 was monitored as index of inflammation. In a fifth group, the effectiveness of intravenous Factor XIII was assessed.

RESULTS

Sodium butyrate, alone or plus mesalamine, reduced histological activity from 13.7 +/- 1.7 (saline) to 2.5 +/- 1.3 and 2.3 +/- 1.1 (P < 0.01), respectively. Transglutaminase, reduced in the colons of the saline group (783 +/- 157 vs. normal 1800 +/- 192 mU/g; P < 0.01), returned toward normal values in the sodium butyrate or sodium butyrate plus mesalamine groups (1390 +/- 228 and 1226 +/- 172 mU/g, respectively; P < 0.01 vs. saline). Furthermore, sodium butyrate plus mesalamine reduced thromboxane B2 levels by day 5 (0.92 +/- 0.16 vs. saline 1.85 +/- 0.34 ng/mL; P < 0.05). Factor XIII therapy improved the histological picture (2.7 +/- 2.1 vs. saline 13.8 +/- 1.7; P < 0.01) and increased transglutaminase levels both in serum (2.81 +/- 0.11 vs. saline 1.45 +/- 0.09 mU/mL; P < 0.01) and in colon (1503 +/- 127 vs. saline 747 +/- 103).

CONCLUSIONS

Sodium butyrate and factor XIII improve colitis, sodium butyrate plus mesalamine reduce early thromboxane B2 synthesis, and transglutaminase(s) plays a role in ulcer healing.

摘要

背景/目的:丁酸盐和凝血因子 XIII 可能改善溃疡性结肠炎;它们还会影响组织和血清转谷氨酰胺酶水平。我们研究了丁酸钠和凝血因子 XIII 的治疗潜力以及转谷氨酰胺酶在实验性结肠炎黏膜修复过程中的作用。

方法

对诱导性结肠炎大鼠分别用丁酸钠、美沙拉嗪、丁酸钠加美沙拉嗪或生理盐水灌肠进行治疗。监测血栓素 B2 作为炎症指标。在第五组中,评估静脉注射凝血因子 XIII 的疗效。

结果

单独使用丁酸钠或丁酸钠加美沙拉嗪可使组织学活性分别从生理盐水组的 13.7±1.7 降至 2.5±1.3 和 2.3±1.1(P<0.01)。转谷氨酰胺酶在生理盐水组结肠中降低(783±157 对比正常组 1800±192 mU/g;P<0.01),在丁酸钠组或丁酸钠加美沙拉嗪组中恢复至正常值(分别为 1390±228 和 1226±172 mU/g;与生理盐水组相比 P<0.01)。此外,丁酸钠加美沙拉嗪在第 5 天时降低了血栓素 B2 水平(0.92±0.16 对比生理盐水组 1.85±0.34 ng/mL;P<0.05)。凝血因子 XIII 治疗改善了组织学表现(2.7±2.1 对比生理盐水组 13.8±1.7;P<0.01),并使血清(2.81±0.11 对比生理盐水组 1.45±0.09 mU/mL;P<0.01)和结肠中的转谷氨酰胺酶水平升高(1503±127 对比生理盐水组 747±103)。

结论

丁酸钠和凝血因子 XIII 可改善结肠炎,丁酸钠加美沙拉嗪可减少早期血栓素 B2 的合成,转谷氨酰胺酶在溃疡愈合中起作用。

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