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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：Sildenafil柠檬酸盐对大鼠实验性结肠炎炎症和细胞凋亡的磷酸二酯酶-5抑制的影响。

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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：探讨西地那非柠檬酸盐（SIL）对结肠炎大鼠组织完整性，氧化剂 - 抗氧化状态和凋亡程度的影响。主要方法：通过Trinitro苯磺酸（TNB）在40％乙醇（30mg / ml; 0.8ml）中诱导结肠炎，以依然鉴定到Sprague-Dawley大鼠。在结肠炎诱导后施用西地那非（25mg / kg /天），继续治疗7天。将其他基团皮下接受N（g） - NiTro-L-精氨酸甲酯（L-名称; 25mg / kg）或N（g） - NiTro-D-精氨酸甲酯（D型; 25 mg / kg）在SIL之前。在斩波之后，将远端结肠进行得分并储存用于测量丙二醛（MDA）水平，谷胱甘肽（GSH）含量，髓氧化酶（MPO）活性和细胞凋亡。通过使用化学发光（CL）监测氧化剂产生。收集血液用于肿瘤坏死因子（TNF） - alpha和白细胞介素（IL）-10测定。主要发现：通过SIL减少结肠炎组的宏观病变评分（P <0.01），L-NAME废除了这种效果（P <0.01）。通过SIL（P <0.01和P <0.001分别）反转结肠MDA的转子MDA的增加随着CONITIN组GSH的伴随的降低。 L-name阻止了SIL对GSH含量的影响（P <0.001）。西地那非还减少了结肠炎组的升高的MPO（P <0.001），L-NAME逆转该效果（P <0.01）。通过SIL（分别为P <0.001和P <0.01），还防止了肠蛋白Cl和血清TNF-α水平的血清TNF-α水平。意义：Sildenafil通过维持氧化剂 - 抗氧化状态，预防细胞凋亡，超氧化物产生和细胞因子释放，Sildenafil部分在TNBS诱导的大鼠结肠炎中受益于TNBS诱导的大鼠结肠炎。

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