广西医学

目的探讨脂联素受体（AdipoR）1和AdipoR2在肥胖相关结肠炎相关性癌（CAC）小鼠结直肠组织中的表达情况。方法（1）将34只雌性昆明小鼠随机分为空白对照组、空白模型组和肥胖模型组。给予空白对照组、空白模型组小鼠饲喂普通饲料，给予肥胖模型组小鼠饲喂高脂饲料；给予空白模型组和肥胖模型组小鼠腹腔注射氧化偶氮甲烷及饮用2%硫酸葡聚糖钠盐以建立CAC模型。最终空白对照组、空白模型组和肥胖模型组分别纳入6只、8只、10只小鼠。（2）记录小鼠一般状态、死亡及成瘤情况，观察小鼠结直肠组织的病理变化，检测小鼠结直肠组织中AdipoR1、AdipoR2 的mRNA及蛋白表达情况。结果（1）空白模型组和肥胖模型组小鼠出现了不同程度的腹泻、脱肛、便血等表现。（2）空白对照组小鼠的死亡比例及成瘤率均为0；空白模型组小鼠的死亡比例为12.5%（1/8），成瘤率为71.4%（5/7）；肥胖模型组的死亡比例为60.0%（6/10），成瘤率为100.0%（4/4）。（3）空白模型组和肥胖模型组小鼠结肠远端出现数量不等的肿瘤，肠黏膜炎症反应明显，结肠黏膜腺体结构紊乱，且肥胖模型组小鼠的上述表现更为严重。（4）与空白对照组相比，空白模型组和肥胖模型组小鼠结直肠组织中AdipoR1、AdipoR2的mRNA表达水平升高，空白模型组小鼠结直肠组织中AdipoR2的蛋白表达水平、肥胖模型组小鼠结直肠组织中AdipoR1及AdipoR2的蛋白表达水平升高（P＜0.05）；与空白模型组相比，肥胖模型组小鼠结直肠组织中AdipoR2的mRNA表达水平、AdipoR1的蛋白表达水平升高（P＜0.05）。结论在CAC小鼠中AdipoR1和AdipoR2的基因和/或蛋白表达上调，且肥胖状态可加重这一现象。脂联素受体对肥胖相关CAC的发生可能发挥重要的调节作用。

ObjectiveTo investigate the expressions of adiponectin receptor (AdipoR)1 and AdipoR2 in colorectal tissues of mice with obesity-associated colitis-associated carcinoma (CAC). Methods(1) A total of 34 female Kunming mice were randomly divided into blank control group, blank model group, or obese model group. General feeds were fed to mice in the blank control and blank model groups, whereas high-fat feeds were fed to mice in the obese model group; in addition, mice in the blank model and obese model groups received intraperitoneal injection of azoxymethane and drank 2% dextran sulfate sodium salt to construct CAC model. Finally, a total of 6, 8, and 10 mice were enrolled in the blank control group, the blank model group, and the obese model group, respectively. (2) The general status, death, and tumor formation states of mice were recorded. The pathological changes of colorectal tissues in mice were observed. The mRNA and protein expressions of AdipoR1 and AdipoR2 in colorectal tissues of mice were detected. Results(1) Mice in the blank model and obese model groups presented as manifestations involving diarrhea, rectocele, and hemafecia, etc.,to various degrees. (2) The proportion of death and tumor formation rate of the blank control group were 0, the proportion of death in the blank model group was 12.5% (1/8), and the tumor formation rate was 71.4% (5/7); furthermore, in the obese model group, the proportion of death was 60.0% (6/10), and the tumor formation rate was 100.0% (4/4). (3) Mice in the blank model and obese model groups presented as a variety of tumors in distal colon, significant intestinal mucosal inflammatory responses, disorder mucosal glandular structure of colon, and mice in the obese model group obtained more severe manifestations as above. (4) Compared with the blank control group, the blank model and obese model groups exhibited elevated mRNA expressions of AdipoR1 and AdipoR2 in colorectal tissues, the blank model group yielded an elevated protein expression of AdipoR2 in colorectal tissues, and the obese model group interpreted elevated protein expressions of AdipoR1 and AdipoR2 in colorectal tissues (P＜0.05). Compared with the blank model group, the obese model group indicated elevated mRNA expression of AdipoR2, and protein expression of AdipoR1 in colorectal tissues (P＜0.05). ConclusionThe gene and/or protein expressions of AdipoR1 and AdipoR2 are up-regulated in CAC mice, and this phenomenon is aggravated by obesity. Adiponectin receptor may play an important regulatory role in the occurrence of obesity-associated CAC.