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首页> 外文期刊>Life sciences >The effect of phosphodiesterase-5 inhibition by sildenafil citrate on inflammation and apoptosis in rat experimental colitis.
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The effect of phosphodiesterase-5 inhibition by sildenafil citrate on inflammation and apoptosis in rat experimental colitis.

机译：枸sil酸西地那非抑制磷酸二酯酶-5对大鼠实验性结肠炎的炎症和细胞凋亡的影响。

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摘要

AIMS: To investigate the effect of sildenafil citrate (SIL) on the extent of tissue integrity, oxidant-antioxidant status and apoptosis in rats with colitis. MAIN METHODS: Colitis was induced by trinitrobenzenesulphonic acid (TNBS) in 40% ethanol (30 mg/ml; 0.8 ml) given intrarectally to Sprague-Dawley rats. Sildenafil (25 mg/kg/day) was administered after the induction of colitis and the treatment was continued for 7 days. Other groups received subcutaneously either N(G)-nitro- L-arginine methyl ester (l-NAME; 25 mg/kg) or N(G)-nitro-d-arginine methyl ester (d-NAME; 25 mg/kg) before SIL. After decapitation, the distal colon was scored and stored for the measurement of malondialdehyde (MDA) level, glutathione (GSH) content, myeloperoxidase (MPO) activity and apoptosis. Oxidant generation was monitored by using chemiluminescence (CL). Blood was collected for tumor necrosis factor (TNF)-alpha and interleukin (IL)-10 assays. KEY FINDINGS: The macroscopic lesion score of the colitis group was reduced by SIL (p < 0.01) and this effect was abolished by l-NAME (p < 0.01). Increase in colonic MDA along with a concomitant decrease in GSH of the colitis group was reversed by SIL (p < 0.01 and p < 0.001, respectively). l-NAME prevented the effect of SIL on GSH content (p < 0.001). Sildenafil also reduced the elevated MPO of the colitis group (p < 0.001) and this effect was reversed by L-NAME (p < 0.01). Increase in lucigenin CL and serum TNF-alpha levels in the colitis group were also prevented by SIL (p < 0.001 and p < 0.01, respectively). SIGNIFICANCE: Sildenafil is beneficial in TNBS-induced rat colitis partially by nitric oxide-dependent mechanisms via the maintenance of oxidant-antioxidant status, prevention of apoptosis, superoxide production and cytokine release.
机译：目的：研究枸sil酸西地那非（SIL）对结肠炎大鼠组织完整性，氧化-抗氧化状态和细胞凋亡程度的影响。主要方法：结肠炎是由三硝基苯磺酸（TNBS）在40％乙醇（30 mg / ml; 0.8 ml）中经直肠给予Sprague-Dawley大鼠所致。诱导结肠炎后给予西地那非（25 mg / kg /天），治疗持续7天。其他组皮下接受N（G）-硝基-L-精氨酸甲酯（l-NAME; 25 mg / kg）或N（G）-硝基-d-精氨酸甲酯（d-NAME; 25 mg / kg）在SIL之前。断头后，对远端结肠进行评分并保存，以测量丙二醛（MDA）水平，谷胱甘肽（GSH）含量，髓过氧化物酶（MPO）活性和细胞凋亡。通过化学发光（CL）监测氧化剂的产生。收集血液用于肿瘤坏死因子（TNF）-α和白介素（IL）-10测定。主要发现：结肠炎组的宏观病变评分被SIL降低（p <0.01），而l-NAME则消除了这种影响（p <0.01）。 SIL逆转了结肠炎组结肠MDA的增加以及GSH的下降（分别为p <0.01和p <0.001）。 l-NAME阻止了SIL对GSH含量的影响（p <0.001）。西地那非还降低了结肠炎组的MPO升高（p <0.001），这种作用被L-NAME逆转（p <0.01）。 SIL也可预防结肠炎组的光泽素CL和血清TNF-α水平升高（分别为p <0.001和p <0.01）。意义：西地那非可通过维持一氧化氮抗氧化剂状态，防止细胞凋亡，超氧化物产生和细胞因子释放，部分通过一氧化氮依赖性机制对TNBS诱导的大鼠结肠炎有益。

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