目的：探讨茶多酚抑制大鼠肾小球系膜细胞摄取氧化型低密度脂蛋白（OX-LDL）的作用。方法：以OX-LDL刺激体外培养的大鼠系膜细胞，同时用不同浓度茶多酚干预，测系膜细胞内总胆固醇（TC）含量，油红-O染色，光染色阳性细胞比例均较无脂蛋白刺激的镜及电镜观察细胞形态。结果：OX-LDL刺激下系膜细胞TC含量及油红-0。照系膜细胞增高，电镜下见泡沫细胞。随培养液茶多酚浓度由40ng L-l～40mg L-1递增，脂蛋白刺激的系膜细胞TC含量及油红-O染色阳性细胞比例递减，呈剂量依赖性关系，系膜细胞内脂滴数量减少。结论：40ng L-1～40mgL-1茶多酚可呈剂量依赖性抑制大鼠系膜细胞摄取OX-LDL。

目的: 探讨核因子2κB（NF2κB）p65在口服耐受发生中的活性改变及其意义。方法: 雌性Wistar大鼠30只随机分成两组：①口服耐受组,用小剂量（每次8mg/2mLPBS）的Fx1A抗原灌胃。②对照组，用PBS2mL/次灌胃。观察大鼠迟发型超敏反应（DTH），进行脾淋巴细胞增殖试验，了解大鼠免疫功能的改变。以免疫组化和ELISA法，检测大鼠淋巴组织中NF-κBp65的活性及TGF-β1的表达。结果：与对照组相比较，口服耐受组大鼠DTH和抗原特异性淋巴细胞增殖反应明显受抑制；肠黏膜 Peyer's淋巴结（PP结）中NF-κB p65 的活性及 TGF-β1的表达明显增加。脾淋巴组织中NF-κB p65 的活性降低，但TGFβ1的表达明显增加。结论：低剂量Fx1A抗原诱导的口服耐受的发生，可能与不同部位免疫细胞内NF-κB p65 的活性改变有关。

AIM: To explore the effct of splenic lymphocytes from oral inr mune tolerance rats on NF-KB p65 actMty in glomerular mesangial cells. METHODS: 10 female Wistar rats with 6-8 weeks of age were divided randomly into two groups, 5 rats for each group. The rats of one group were given through intragastric feeding with 2 mL FxlA antigen to induce oral inr mune tolerance, and the rats of the other group only with PBS (as control group). Two weeks later, the rats were sacrficed, and then their spleens were excised and lymphocytes were sey arated routinely for antigerrspecific lymphocytes reaction. The cukure supernatants of splenic lymphocytes from oral immune tolerance rats were prepared. The L-10 level in the super natants was detected by sandwich FLISA. After the cultured mesangial cells were stimulated with high dose of insulin, the culture supernatants of rat's splenic lymphocytes were added to insulin-treated mesangial cells. Twentyfour hours later, the NF KB p65 actMty in mesangial cells was detected by immunohisto-chemical staining and sandwich ELISA. RESULTS: As com- pared with control group, the proWeration reaction of splenic lymphocytes from oralimmune tolerance rats was inhibited obvr ously, and lL-10 level in splenic lymphocyte culture supernatants from the tolerance rats rose markedly (P<0.01). NF-KB p65 actMty induced by insulin in me sangial cells wa s inhibited by cul-ture superatants of splenic lymphocytes from oralimmune toter ance rats (P<0.05). CONCLUSION: NF-KB p65 actMty in mesangial cells may be inhibited by lL-10 secreted by splenic lymphocytes from the oral immune tolerance rats.

目的探讨口服诱导免疫耐受对主动性Heymann肾炎（AHN）的防治作用及机制。方法6～8周龄Wistar雌性大鼠30只平均分3组，AHN模型组和口服诱导免疫耐受组大鼠分别予PBS、FxlA灌胃，然后皮下免疫FxlA/CFA，同时设正常对照组。观察大鼠迟发性超敏反应（DTH）、肾组织的病理变化、尿蛋白水平，并用Sandwich ELISA法和免疫组化染色分别观察大鼠脾淋巴组织和肾小球内核因子NF-KB p65的活化。结果与正常对照组大鼠比较，AHN模型组和口服诱导免疫耐受组大鼠迟发性超敏反应均明显增强，肾小球基底膜（GBM）明显增厚、尿蛋白水平明显增多，肾小球内和脾淋巴组织NF-KB p65的活化明显增加，但与AHN模型组比较，口服诱导免疫耐受组DTH明显减低，尿蛋白水平减低，肾组织病变程度和NF-KB p65的活化程度有所减轻，差异有显著性（P<0.01）；肾小球内NF-KB p65的阳性细胞数与脾淋巴组织NF-KB p65活性和肾小球基底膜厚度呈明显的直线正相关（P<0.05）。结论口服诱导免疫耐受臧轻了AHN肾小球的病理损害，可能与口服诱导免疫耐受对脾淋巴细胞和肾小球内细胞NF-nB p65的活化的抑制作用有关。