生地、山茱萸抑制和清除糖基化产物的效应成分研究

目的:糖基化终末产物(AGEs)是糖尿病的主要物质基础,在加速糖尿病及其并发症的进程中发挥了核心作用,本实验观察生地、山茱萸效应成分对体外AGEs生成与清除的影响。方法:加入葡萄糖(终浓度为200mmol/L)和牛血清白蛋白(终浓度40g/L)37℃温孵2周后,于530nm处测定早期糖化蛋白(果糖胺);37℃温孵4周后于激发波长360nm,发射波长460nm处测定AGEs的荧光度值(F),建立体外AGEs生成模型;加入葡萄糖(终浓度为200mmol/L)和牛血清白蛋白(终浓度40g/L)后37℃温孵16h,采用酶联免疫吸附测定法,于450nm处测定OD值,建立AGEs清除模型。再分别加入生地效应成分(梓醇、水苏糖、毛蕊花糖苷),山茱萸效应成分(马钱苷、莫诺苷、熊果酸、齐墩果酸、獐牙菜苷),使其终浓度为1×10-5、5×10-6、1×10-6、5×10-7、1×10-7mol/L;氨基胍(1×10-5、5×10-6、1×10-6、5×10-7、1×10-7mol/L)作阳性对照。结果:在体外AGEs生成模型中,发现生地梓醇、水苏糖,山茱萸熊果酸对果糖胺抑制作用较强,IC50分别为4.2×10-8、9.4×10-8、5.7×10-8,而山茱萸马钱苷对AGEs生成的抑制作用较强,IC50为6.1×10-7。在体外AGEs清除模型中,发现山茱萸有效成分熊果酸、生地有效成分毛蕊花糖苷抑制作用最强,浓度为1×10-5mol/L时,抑制率分别为16.8%、17.4%。结论:生地、山茱萸各特征成分对抑制AGEs生成和清除AGEs交联结构都有一定的作用,但各有效成分作用靶点、作用环节不同,为生地、山茱萸两药合用在临床上治疗糖尿病及并发症提供了有效的依据。

山茱萸、生地有效部位及配伍组合抑制糖基化终末产物致肾小球系膜细胞增殖的研究

目的：通过体外培养大鼠肾小球系膜细胞（GMC）,建立糖基化终末产物（AGEs）致肾小球系膜细胞增殖的细胞模型,观察山茱萸有效部位、生地有效部位及其配伍组合对糖基化终末产物致肾小球系膜细胞增殖的抑制作用,以确定最佳配伍组合物。方法：体外培养肾系膜细胞,当细胞贴壁生长至80%-90%时,（1）,用浓度为50、100、200、400mg/L的山茱萸各部位（环烯醚萜苷、三萜酸、多糖）、生地各部位（环烯醚萜苷、多糖、寡糖）进行干预,然后加入200mg/L的糖基化终末产物刺激,24 h后检测细胞增殖情况,筛选出活性较强的部位。（2）,将活性较强的部位山茱萸环烯醚萜苷和三萜酸（A）、生地环烯醚萜苷（B）按1：0、0：1、1：1、1：2、2：1进行配伍组合（分别为A1、B1、A1B1、A1B2、A2B1）,以浓度为25、50、100mg/L生药及含药血清进行干预,加入200mg/L的AGEs刺激,24 h后检测细胞增殖情况以及细胞上清液中纤维连接蛋白（FN）、层粘连蛋白（LN）、Ⅳ型胶原（Coll-Ⅳ）水平。结果：（1）山茱萸环烯醚萜苷部位、山茱萸三萜酸部位与生地环烯醚萜苷部位活性较强,具有显著抑制糖基化终末产物致肾小球系膜细胞增殖的作用。（2）配伍组合物（A1、B1、A1B1、A1B2、A2B1）生药及含药血清均能够抑制肾小球系膜细胞增殖及其分泌纤维连接蛋白、层粘连蛋白、Ⅳ型胶原的水平,并呈一定量效关系。结论：山茱萸环烯醚萜苷部位、山茱萸三萜酸部位、生地环烯醚萜苷部位及其配伍组合能够明显抑制糖基化终末产物致肾系膜细胞增殖及其分泌的纤维连接蛋白、层粘连蛋白、Ⅳ型胶原水平,减少细胞外基质沉积,其中配伍组合A2B1抑制效应最强,为最佳配伍组合。

山茱萸多糖对血管性痴呆大鼠抗氧化作用的研究

目的:通过建立大鼠血管性痴呆模型,研究山茱萸多糖对血管性痴呆大鼠学习记忆、脑组织氧化应激反应的影响。方法:将雄性SD大鼠60只,随机分为6组,包括假手术组、模型组、山茱萸多糖0.14g/kg、0.28g/kg、0.56g/kg组和盐酸多奈哌齐0.52mg/kg组。除假手术组外,其余各组均制备血管性痴呆模型,其中假手术组与模型组每天灌胃生理盐水,其余各组分别连续28天灌胃不同剂量山茱萸多糖和盐酸多奈哌齐。28天后,分别对6组大鼠行morris水迷宫测试,测试完成后,断头取脑,测定脑组织中单胺氧化酶(MAO)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)含量。结果:morris水迷宫测试结果显示,随着训练时间延长各组大鼠逃避潜伏期时间逐渐变短,0.28g/kg、0.56g/kg山茱萸多糖组大鼠平均逃避潜伏期明显缩短;空间探索试验中,与模型组比较,0.28g/kg、0.56g/kg山茱萸多糖组大鼠在平台象限路径百分比与平台象限停留时间明显长于模型组。与假手术组相比,模型组脑组织GSH-Px、CAT活性明显下降,MAO活性明显升高;与模型组相比,0.28g/kg、0.56g/kg山茱萸多糖组大鼠脑组织GSH-Px、CAT活性明显升高,MAO活性明显下降。结论:山茱萸多糖能够明显提高血管性痴呆大鼠学习记忆能力,其作用机制可能通过对抗机体氧化应激。

山茱萸总苷对急性缺氧乳鼠心肌细胞凋亡通路的影响

目的:探讨山茱萸总苷对急性缺氧乳鼠心肌细胞凋亡通路的影响。方法:原代培养乳鼠的心肌细胞,采用液体石蜡封闭法建立缺血缺氧模型,并将原代培养3天的心肌细胞分为正常组、缺氧组(1h、2h、3h、5h)及药物治疗组,药物浓度采用山茱萸总苷三个剂量组,免疫组化法检测各组cleaved caspase-9表达。结果:与对照组相比,缺氧各组caspase-9表达增加(P<0.01),并且随着时间延长,阳性表达的比例增加,5h达到最高,给予山茱萸总苷干预之后,治疗组每个时间点cleaved caspase-9表达都有所下降,随着山茱萸总苷剂量的增加,cleaved caspase-9表达逐渐下降,与缺氧组相比,没有统计学意义,但0.049g/L和0.49g/L组差异有统计学意义(P<0.01)。山茱萸总苷起效剂量为0.049g/L,剂量范围为0.049g/L^0.49g/L。结论:山茱萸总苷可以抑制cleaved caspase-9的表达,可能是通过阻断心肌细胞凋亡线粒体通路去实现对心肌细胞起保护作用。

Paleocene Wuyun Flora in Northeast China: Amersinia and Beringiaphyllum of Cornaceae sensu

Specimens of Amersinia obtrullata and Beringiaphyllum pseudoantiquum in Paleocene Wuyun flora, Heilongjiang Province, Northeast China, were described and assigned to Cornaceae sensu. Infructescences formally allocated in Trochodendron sp. were reviewed and assigned to Amersinia obtrullata. Leaves described as Populus carneosa, Celastrophyllum subprotophyllum, Viburnum antiquum, V. asperum, Viburniphyllum finale, Protophyllum wuyunense, P. cf. haydenii, P. ovatifolium, Credneria inordinata were also restudied and assigned to Beringiaphyllum pseudoantiquum.

《人民周刊》特稿:总书记走过的村庄 香包里的马庄音乐

2017年12月12日下午,习近平总书记来到江苏徐州马庄村,看到村民们手工制作的特色香包,连连称赞＂真不错＂＂很精致＂。80岁的村民王秀英递上自己制作的中药香包,习近平问：＂多少钱？我买一个,捧捧场。＂＂不要钱,送给总书记。＂王秀英答道。习近平还是坚持付了30元。

Effect of Cornus officinalis glycoside on adjuvant-induced arthritis in rats

The aim of this study was to explore the effect of Comus officinalis glucosides （COG） on adjuvant-induced arthritis in rats and its mechanism. Seventy-two rats were divided into six groups of norreal, model, Dexasone （0. 125 mg/kg）, high-dose COG （240 mg/kg）, mid-dose COG （120 mg/kg）, and low-dose COG （60 mg/kg）. Rat arthritis was induced by injection of Freund＇s complete adjuvant in the hind paws. All treatment started from the day the arthritis was induced. The edema degree of the adjuvant injection location was determined on days 1, 3, 5, 7, 9, 11, 13, 15, 17, 20, 23 and the oppo- site side was observed on days 11, 13, 15, 17, 20, 23 after the injection of adjuvant. All rats were sacrificed on day 24 after the injection of adjuvant for microscopic examination of the ankle, and for the study of the immunological molecular mechanism. The results showed that the COG significantly suppressed both the primary and secondary edema, improved pathological injuries of adjuvant arthritis （AA） rat ankles, significantly suppressed the proliferation of T lymphocytes and DTH reaction. It significantly suppressed IL-1, IL-6 and TNF-α production from peritoneal macrophages and PGE2 in plasma. In conclusion, the Comus officinalis glucosides （COG） is able to prevent and cure the rat adjuvant-induced arthritis, and can suppress the production of pro-inflammatory cytokine IL-1, IL-6, TNF-α and PGE2.

Research progress on the chemical constituents and pharmacological activities of Fructus corni

Fructus corni is the dried sarcocarp of Cornus officinalis Sieb.et Zucc.It has been used as an important traditional Chinese medicine.Its action is to protect liver and kidney and regulate the essence of human body.In this paper,the research progress on the chemical ingredients and pharmacological activities of Fructus corni are reviewed.According to its pharmacological activities,some suggestions for future research and development have been made.

Effect of 5-HMF on protection of hydrogen peroxide-induced injury in human umbilical vein endothelial cells

The protective effect of 5-hydroxymethylfurfural（5-HMF） against hydrogen peroxide（H2O2）-induced injured in human umbilical vein endothelial cells（HUVECs） was examined. Treatment of HUVECs with 5-HMF significantly increased their viability, decreased cell apoptosis induced by H2O2, accompanied by the decreased nitric oxide level. Western blotting analysis demonstrated that Bcl-2 expression was increased whereas Caspase-3 and NF-κB expression was decreased in 5-HMF groups. In conclusion, the results showed that 5-HMF could prevent endothelial dysfunction and related complications caused by oxidative stress.