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目的观察氧化苦参碱对宫颈癌HeLa细胞侵袭转移的作用及其相关分子机制。方法 MTT法检测氧化苦参碱的抗增殖活性;Transwell小室法检测氧化苦参碱对HeLa细胞增殖的影响;Real-time PCR法检测氧化苦参碱对宫颈癌HeLa细胞侵袭转移能力的影响;Western blot法检测氧化苦参碱对MMP-2、MMP-9、AKT及p-AKT表达水平的影响。结果氧化苦参碱能够有效抑制HeLa细胞的增殖,与对照组（0mg/mL）相比,氧化苦参碱高于0.8mg/mL时出现明显差异。低于细胞毒性浓度（0.8mg/mL）的氧化苦参碱能够明显抑制HeLa细胞的侵袭能力,随着氧化苦参碱浓度的升高穿过基质胶到达小室底端的细胞数目明显减少,0.1、0.2和0.4mg/mL组分别为对照组的（77.07±20.43）%、（53.95±18.17）%、（20.35±11.20）%;0.1、0.2、0.4mg/mL组MMP-2的RNA水平分别为对照组的（82.76±8.71）%、（39.51±12.79）%、（21.53±5.38）%,0.4mg/mL组MMP-2的蛋白水平为对照组的（64.69±16.52）%;0.4mg/mL组AKT的磷酸化水平为对照组的（41.27±7.13）%。结论氧化苦参碱能够明显抑制宫颈癌HeLa细胞的侵袭转移,这种作用可能是通过调节AKT信号通路的活性进而调节MMP-2的表达来实现的。本研究为氧化苦参碱的抗肿瘤机制增添了新的内容。

目的观察氧化苦参碱对慢性肾脏病（CKD）患者血清转化生长因子-β1（TGF-β1）、Ⅲ型胶原（ColⅢ）的影响，探讨其在肾间质纤维化发生发展过程中的作用和治疗价值。方法选取健康对照者10例、慢性肾脏病患者40例，根据肾小球滤过率（GFR）分为轻度肾损害组（GFR〈90mL／min·1．73m^2，CKDI）、中重度肾损害组（GFR〈60mL／min·1．73m^2，CKDⅡ），再分层随机抽样，分为常规治疗组和氧化苦参碱组。利用双抗体夹心酶联免疫吸附法分别检测各研究对象治疗前、后血清TGF-β1、ColⅢ含量，采用t检验比较两组TGF-β1、ColⅢ水平的差异。站果氧化苦参碱组TGF-β1、ColⅢ含量显著低于常规治疗组（P〈0．05）。站论氧化苦参碱可能通过下调TGF-β1、ColⅢ水平，减少ECM沉积，从而达到防止肾间质纤维化的作用。

目的观察氧化苦参碱对慢性肾脏病（CKD）患者血清基质金属蛋白酶-9（MMP-9）、基质金属蛋白酶组织抑制因子-1（TIMP-1）的影响,探讨其在肾间质纤维化发生发展过程中的作用和治疗价值。方法选取健康对照者10例、慢性肾脏病患者40例,根据肾小球滤过率（GFR）分为轻度肾损害组（GFR〈90 mL/min.1.73 m2,CKDⅠ）和中、重度肾损害组（GFR〈60 mL/min.1.73 m2,CKDⅡ）,再分层随机抽样,分为常规治疗组和氧化苦参碱组。利用双抗体夹心酶联免疫吸附法分别检测各组治疗前后血清MMP-9和TIMP-1含量,采用t检验比较两组MMP-9和TIMP-1水平的差异。结果经氧化苦参碱干预后,TIMP-1水平显著低于常规治疗组,而MMP-9水平则显著高于常规治疗组（P〈0.05）。结论氧化苦参碱可下调TIMP-1水平,恢复MMP-9水平,保持MMP-9/TIMP-1平衡,减少细胞外基质（ECM）沉积,防止肾间质纤维化。

目的 探讨氧化苦参碱对大鼠肾间质纤维化进程的干预作用，并阐明其部分机制。方法 40只雄性SD大鼠，随机分为假手术组、模型组、苯那普利组、氧化苦参碱大剂量组和小剂量组。以单侧输尿管结扎术建立输尿管梗阻的动物模型。术后第14天取术侧肾组织行HE、Masson染色及转化生长因子-β1（TGF-β1）、α-平滑肌肌动蛋白（α—SMA）和Ⅲ型胶原（ColⅢ）免疫组化检测，并运用图像分析系统做半定量分析。结果 经氧化苦参碱干预后，梗阻侧肾脏的α—SMA、TGF—β1和ColⅢ的表达均显著低于模型组（P〈0．01）；大剂量氧化苦参碱组均低于苯那普利组（P〈0．05）；氧化苦参碱大剂量组和小剂量组之间无显著性差异（P〉0．05）。结论 氧化苦参碱可能是通过降低TGF-β1等细胞因子的表达而减少细胞外基质（ECM）产生细胞的活化，从而减少ECM的沉积，达到抗肾间质纤维化的作用。

Kushen （Radix Sophorae Flavescentis） has a long history of use for the treatment of tumors, inflammation and other diseases in traditional Chinese medicine. Compound Kushen Injection （CKI） is a mixture of natural compounds extracted from Kushen and Baituling （Rhizoma Smilacis Glabrae）. The main principles of CKI are matrine （MT） and oxymatrine （OMT） that exhibit a variety of pharmacological activities, including anti-inflammatory, anti-allergic, anti-viral, anti-fibrotic and cardiovascular protective effects. Recent evidence shows that these compounds also produce anti-cancer actions, such as inhibiting cancer cell proliferation, inducing cell cycle arrest, accelerating apoptosis, restraining angiogenesis, inducing cell differentiation, inhibiting cancer metastasis and invasion, reversing multidrug resistance, and preventing or reducing chemotherapy- and/or radiotherapy-induced toxicity when combined with chemotherapeutic drugs. In this review, we summarize recent progress in studying the anti-cancer activities of MT, OMT and CKI and their potential molecular targets, which provide clues and references for further study.

Aim： Oxymatrine （OMT） is the major quinolizidine alkaloid extracted from the root of Sophora flavescens Ait （the Chinese herb Kushen） and exhibits diverse pharmacological actions. In this work we investigated the effects of OMT on diabetes-associated cognitive decline （DACD） in a rat model of diabetes and explored the mechanisms of action. Methods： Male Wistar rats were injected with streptozotocin （65 mg/kg, ip） once to induce diabetes. The rats were then treated with vehicle or OMT （60 or 120 mg/kgper day, ip） for 7 weeks. Memory function was assessed using Morris water maze test. The levels of malondialdehyde （MDA）, superoxide dismutase （SOD）, glutathione （GSH）, NF-KB p65 unit, TNF-a, IL-113 and caspase-3 in the cerebral cortex and hippocampus were quantified. Results： The diabetic rats exhibited markedly reduced body weight and increased plasma glucose level. The memory function of the rats assessed using Morris water maze test showed significant reduction in the percentage of time spent in the target quadrant and the number of times crossing the platform, coupled with markedly prolongation of escape latency and mean path length. Moreover, the rats showed oxidative stress （significantly increased MDA, decreased SOD and reduced GSH levels）, as well as significant increases of NF-KB p65 unit, TNF-（x, IL-113 and caspase-3 lew.~ls in the cerebral cortex and hippocampus. Chronic treatment with OMT dose- dependently reversed these behavioral, biochemical and molecular changes in the diabetic rats. However, the swimming speed had no significant difference among the control, diabetic and OMT-treated diabetic rats. Conclusion： Chronic treatment with OMT alleviates diabetes-associated cognitive decline in rats, which is associated with oxidative stress, inflammation and apoptotic cascades.