稳定型胃五肽bpc157、L-NAME和l -精氨酸对大鼠肠粘连的治疗作用。

Lidija Berkopic Cesar, Slaven Gojkovic, Ivan Krezic, Dominik Malekinusic, Helena Zizek, Lovorka Batelja Vuletic, Andreja Petrovic, Katarina Horvat Pavlov, Domagoj Drmic, Antonio Kokot, Josipa Vlainic, Sven Seiwerth, Predrag Sikiric
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引用次数: 10

摘要

背景:大鼠腹膜壁层切除后,皮下有浅层肌肉组织,血管系统衰竭,最后,粘连形成增加。我们假设,与一氧化氮(NO)药物、L-NAME和/或l -精氨酸不同,稳定的胃五肽BPC 157及其最新血管效应(“血管招募”)的应用意味着肠道粘连形成和NO-和丙二醛(MDA)组织值的减弱。目的:探讨bpc157在肠粘连中的应用及其在no类药物中的应用。方法:随着缺陷的产生,用药:(1)术中,1次,在缺陷产生后1分钟腹腔浴(1 mL/大鼠),BPC 157(10µg/kg, 10 ng/kg, 1 mL/大鼠),等量生理盐水,L-NAME (5 mg/kg), l -精氨酸(200 mg/kg)单独和/或联合。另外,(2)每日一次腹腔注射,手术后30分钟首次给药,最后一次给药,7天或14天评估前24小时给药。作为对预先存在的粘连的延迟治疗(3),BPC 157(10µg/kg, 10 ng/kg腹腔注射,1 mL/大鼠)从第7天起每天给予1次。结果:bpc157方案的修复效果与缺损内及缺损附近血管丰富、发生迅速密切相关。最后,也作为后处理应用,bpc157产生弱粘连,最小或无粘连。相反,NO-agents具有不同的初始和最终效果:血管消失的初始减弱,最后粘连的严重恶化(L-NAME)与血管消失的初始减弱,最后粘连形成的衰减(l -精氨酸),两者相互抵消。重要的是,bpc157与NO-agents (L-NAME + bpc157;l -精氨酸+ bpc157;L-NAME + l -精氨酸+ bpc157)。最后,在NO-和MDA-值升高与粘附组织形成的关系方面,与NO-制剂的多种作用不同,BPC 157的应用效果通常是降低NO-和MDA-值升高与有益结果(减少粘附形成)相结合的。结论:bpc157治疗可有效实现腹膜缺损的愈合,且无粘连或极少粘连形成。
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Bowel adhesion and therapy with the stable gastric pentadecapeptide BPC 157, L-NAME and L-arginine in rats.

Background: After parietal peritoneum excision with an underlying superficial layer of muscle tissue in rats, there is failed vasculature, and finally, increased adhesion formation. We hypothesized that unlike nitric oxide (NO)-agents, L-NAME and/or L-arginine, the application of the stable gastric pentadecapeptide BPC 157 with its most recent vascular effects ("vascular recruitment") means attenuated bowel adhesion formation and NO- and malondialdehyde (MDA)-tissue values.

Aim: To focused on the bowel adhesion and the therapy with the BPC 157, its most and application of NO-agents.

Methods: Along with defect creation, medication was (1) during surgery, once, at 1 min after defect creation as an abdominal bath (1 mL/rat), BPC 157 (10 µg/kg, 10 ng/kg, 1 mL/rat), an equivolume of saline, L-NAME (5 mg/kg), L-arginine (200 mg/kg) alone and/or combined. Alternatively, medication was (2) intraperitoneally once daily, first application at 30 min after surgery, last application 24 h before assessment at d 7 or d 14. As a postponed therapy to pre-existing adhesion (3), BPC 157 (10 µg/kg, 10 ng/kg intraperitoneally, 1 mL/rat) was given once daily since d 7.

Results: The recovery effect of the BPC 157 regimens goes with the presence of abundant vascular vessels in and near the defect, which occurs rapidly. Lastly, also applied as post-treatment, BPC 157 creates attenuated adhesions, minimal or no adhesion. Contrarily, NO-agents have diverse initial and final effects: The initial weakening of blood vessel disappearance and finally, severe worsening of adhesions (L-NAME) vs the initial weakening of blood vessel disappearance and finally, attenuation of adhesions formation (L-arginine), which counteract each other response given together. Importantly, BPC 157 maintains its beneficial effect also when given with NO-agents (L-NAME + BC 157; L-arginine + BPC 157; L-NAME + L-arginine + BPC 157). Finally, with respect to the increased NO- and MDA- values-adhesion tissue formation relation, unlike diverse effect of the NO-agents, the BPC 157 application effect regularly combines decrease on the increased NO- and MDA- values and the beneficial outcome (less adhesion formation).

Conclusion: BPC 157 therapy can be suited for the realization of the peritoneal defect healing with minimal or no adhesion formation.

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