Inflammatory bowel disease composed of ulcerative colitis and Crohn’s disease is a disorder that may involve entire gastrointestinal tract. Its pathogenesis is mainly an immune-mediated inflammation. Recently, it has been indicated that bupropion possesses anti-inflammatory properties; hence, the objective of this experiment is the investigation of the anti-inflammatory influence of bupropion on colonic lesions that emerged following the intrarectal administration of acetic acid. Thirty-six male Wistar rats were allocated randomly into six groups, including control, acetic acid, dexamethasone (2 mg/kg), and bupropion (40, 80, and 160 mg/kg). Colitis was induced by intrarectal administration of acetic acid in all study groups except control group, and animals were treated by oral administration of dexamethasone and bupropion. While macroscopic and microscopic lesions were observed after colitis induction, administration of dexamethasone and bupropion 160 mg/kg led to the remarkable improvement in lesions. In addition, the expression of TLR4 and NF-ĸB was decreased after colitis induction; however, treatment with dexamethasone (2 mg/kg) and bupropion (160 mg/kg) resulted in a significant decrease in their expression. Regarding biochemical factors, following colitis induction, TNF-α level and MPO activity were increased; nevertheless, dexamethasone (2 mg/kg) and bupropion (160 mg/kg) decreased the TNF-α and MPO activity. In conclusion, bupropion exerts anti-inflammatory influence through suppressing the TLR4 and NF-ĸB expression in the rat model of acute colitis.

由溃疡性结肠炎和克罗恩氏病组成的炎性肠病是一种疾病，可能涉及整个胃肠道。其发病机理主要是免疫介导的炎症。近来，已表明安非他酮具有抗炎特性。因此，本实验的目的是研究安非他酮对直肠内施用乙酸后出现的结肠病变的抗炎作用。将36只Wistar雄性大鼠随机分为6组，包括对照组，醋酸，地塞米松（2 mg / kg）和安非他酮（40、80和160 mg / kg）。除对照组外，所有研究组均通过直肠内注射乙酸诱发结肠炎，并通过口服地塞米松和安非他酮治疗动物。诱发结肠炎后可观察到宏观和微观病变，但地塞米松和安非他酮160 mg / kg的使用可明显改善病变。此外，结肠炎诱导后TLR4和NF-ĸB的表达降低。然而，地塞米松（2 mg / kg）和安非他酮（160 mg / kg）治疗导致其表达显着下降。在生化因素方面，诱导结肠炎后，TNF-α水平和MPO活性升高。然而，地塞米松（2 mg / kg）和安非他酮（160 mg / kg）降低了TNF-α和MPO活性。总之，安非他酮通过抑制急性结肠炎大鼠模型中的TLR4和NF-ĸB表达来发挥抗炎作用。地塞米松和安非他酮160 mg / kg的使用可显着改善病灶。此外，结肠炎诱导后TLR4和NF-κB的表达降低。然而，地塞米松（2 mg / kg）和安非他酮（160 mg / kg）治疗导致其表达显着下降。在生化因素方面，诱导结肠炎后，TNF-α水平和MPO活性升高。然而，地塞米松（2 mg / kg）和安非他酮（160 mg / kg）降低了TNF-α和MPO活性。总之，安非他酮通过抑制急性结肠炎大鼠模型中的TLR4和NF-ĸB表达来发挥抗炎作用。地塞米松和安非他酮160 mg / kg的使用可显着改善病灶。此外，结肠炎诱导后TLR4和NF-κB的表达降低。然而，地塞米松（2 mg / kg）和安非他酮（160 mg / kg）治疗导致其表达显着下降。在生化因素方面，诱导结肠炎后，TNF-α水平和MPO活性增加；然而，地塞米松（2 mg / kg）和安非他酮（160 mg / kg）降低了TNF-α和MPO活性。总之，安非他酮通过抑制急性结肠炎大鼠模型中的TLR4和NF-ĸB表达来发挥抗炎作用。地塞米松（2 mg / kg）和安非他酮（160 mg / kg）处理导致其表达显着下降。在生化因素方面，诱导结肠炎后，TNF-α水平和MPO活性增加；然而，地塞米松（2 mg / kg）和安非他酮（160 mg / kg）降低了TNF-α和MPO活性。总之，安非他酮通过抑制急性结肠炎大鼠模型中的TLR4和NF-ĸB表达来发挥抗炎作用。地塞米松（2 mg / kg）和安非他酮（160 mg / kg）处理导致其表达显着下降。在生化因素方面，诱导结肠炎后，TNF-α水平和MPO活性升高。然而，地塞米松（2 mg / kg）和安非他酮（160 mg / kg）降低了TNF-α和MPO活性。总之，安非他酮通过抑制急性结肠炎大鼠模型中的TLR4和NF-ĸB表达来发挥抗炎作用。