Ercan Gulcin, Yigitturk Gurkan, Erbas Oytun
MD, Department of General Surgery, University of Health Science Bagcilar Training and Research Hospital, Istanbul, Turkey. Scientific, intellectual, conception and design of the study; technical procedures; analysis and interpretation of data; manuscript writing; critical revision, final approval.
PhD, Department of Histology and Embryology, Faculty of Medicine of Mugla Sitki Kocaman University, Mugla, Turkey. Acquisition, analysis and interpretation of data; technical procedures; histopathological examinations; critical revision; final approval.
Acta Cir Bras. 2020 Feb 14;34(12):e201901204. doi: 10.1590/s0102-865020190120000004. eCollection 2020.
To examine the therapeutic effect of external adenosine on an acetic acid-induced acute ulcerative colitis model in rats.
Thirty male mature rats were divided into three groups as control, acute colitis (AC) and AC+adenosine group (AC+AD). AC was induced by rectal administration of 4% acetic acid (AA). 5mg/kg/day adenosine was performed i.p for 4 weeks to AC+AD group. Rectum and colon were excised for microscopic and histopathological histopathologic evaluations, and immunohistochemical analysis of nuclear factor kappa B (NF-kB). Blood samples were collected for biochemical detection of TNF-α, Pentraxin-3 and malondialdehyde (MDA) levels.
AC group had generalized hyperemia and hemorrhage with increased macroscopic and histopathological scores compared with control (P <0.0001) while adenosine treatment decreased these scores significantly (P <0.001), with reduced distribution of disrupted epithelium, leukocyte infiltrates, and focal hemorrhage. AC group showed significantly increased immunoexpression of NF-kB in rectum, plasma and tissue levels of TNF-α, plasma Pentraxin-3 and MDA levels (P <0.0001) while adenosine reduced these levels (P < 0.05).
Adenosine appears to promote healing of colon and rectum exposed to AA-induced AC, suggesting a boosting effect of adenosine on the intestinal immune system to cure ulcerative colitis.
研究外源性腺苷对大鼠乙酸诱导的急性溃疡性结肠炎模型的治疗效果。
将30只雄性成年大鼠分为三组,即对照组、急性结肠炎(AC)组和AC+腺苷组(AC+AD)。通过直肠给予4%乙酸(AA)诱导AC。对AC+AD组腹腔注射5mg/kg/天的腺苷,持续4周。切除直肠和结肠进行微观和组织病理学评估,以及核因子κB(NF-κB)的免疫组织化学分析。采集血样用于检测肿瘤坏死因子-α(TNF-α)、五聚素-3和丙二醛(MDA)水平的生化检测。
与对照组相比,AC组出现广泛充血和出血,宏观和组织病理学评分增加(P<0.0001),而腺苷治疗显著降低了这些评分(P<0.001),上皮破坏、白细胞浸润和局灶性出血的分布减少。AC组直肠中NF-κB的免疫表达、TNF-α的血浆和组织水平、血浆五聚素-3和MDA水平显著升高(P<0.0001),而腺苷降低了这些水平(P<0.05)。
腺苷似乎能促进暴露于AA诱导的AC的结肠和直肠愈合,提示腺苷对肠道免疫系统有增强作用以治愈溃疡性结肠炎。