Miampamba M, Parr E J, McCafferty D M, Wallace J L, Sharkey K A
Department of Physiology and Biophysics, University of Calgary, Alberta, Canada.
Aliment Pharmacol Ther. 1998 Mar;12(3):219-28. doi: 10.1046/j.1365-2036.1998.00311.x.
We investigated the effects of benzalkonium chloride (BAC) on trinitrobenzene sulphonic acid (TNBS)-induced colitis in rats.
TNBS was administered intrarectally before and/or after BAC treatment. In the first study, the effects of treatment with BAC 6, 12 or 24 h after TNBS were examined. In the second study, animals were treated with BAC before, after or before and after TNBS, and were examined 7 days later. The severity of colitis was assessed by macroscopic and histological scoring of the colonic damage and by determination of colonic myeloperoxidase (MPO) activity. Macrophages and CD4+ and CD8+ T cells were examined by immunohistochemistry.
When BAC was instilled into the colon 6, 12 or 24 h after TNBS, weight loss and macroscopic and histological features of the colon were similar to that of controls (TNBS alone). In contrast, MPO activity was significantly reduced in all three groups post-treated with BAC. In the groups examined 7 days after TNBS treatment, rats post-treated with BAC exhibited increased weight gain and significantly reduced macroscopic damage and MPO activity compared to the TNBS control group. Rats pre-treated with BAC exhibited less macroscopic damage of the colon than rats receiving only TNBS, but histological damage, MPO and weight gain were unchanged from TNBS controls. Immunohistochemistry revealed that BAC pre-treatment increased the numbers of macrophages and T cells in the colon. After TNBS treatment, macrophage accumulation was evident in the colon, but T cells were scarce. However, these cells were preserved or enhanced in the colonic mucosa in TNBS-treated rats that had been pre-treated with BAC.
Treatment with BAC, particularly after induction of colitis, produces a significant reduction in the severity of tissue injury and inflammation through mechanisms that are not fully understood.
我们研究了苯扎氯铵（BAC）对三硝基苯磺酸（TNBS）诱导的大鼠结肠炎的影响。
在BAC治疗之前和/或之后经直肠给予TNBS。在第一项研究中，检测了TNBS后6、12或24小时给予BAC治疗的效果。在第二项研究中，动物在TNBS之前、之后或之前及之后接受BAC治疗，并在7天后进行检查。通过对结肠损伤进行宏观和组织学评分以及测定结肠髓过氧化物酶（MPO）活性来评估结肠炎的严重程度。通过免疫组织化学检查巨噬细胞以及CD4 +和CD8 + T细胞。
当在TNBS后6、12或24小时将BAC注入结肠时，体重减轻以及结肠的宏观和组织学特征与对照组（仅TNBS组）相似。相比之下，所有三组BAC治疗后MPO活性均显著降低。在TNBS治疗7天后检查的组中，与TNBS对照组相比，BAC治疗后的大鼠体重增加增加，宏观损伤和MPO活性显著降低。预先用BAC治疗的大鼠结肠的宏观损伤比仅接受TNBS的大鼠少，但组织学损伤、MPO和体重增加与TNBS对照组相比没有变化。免疫组织化学显示，BAC预处理增加了结肠中巨噬细胞和T细胞的数量。TNBS治疗后，结肠中巨噬细胞明显积聚，但T细胞稀少。然而，在预先用BAC治疗的TNBS处理的大鼠的结肠黏膜中，这些细胞得以保留或增加。
BAC治疗，特别是在结肠炎诱导后，通过尚未完全了解的机制显著降低了组织损伤和炎症的严重程度。
