云南省19个县(市)印度囊棒恙螨的分布调查

目的 探讨云南省印度囊棒恙螨在不同宿主、不同地域及其不同生境的分布情况.方法 选择云南省19个县(市)进行现场调查,用鼠笼加食饵诱捕小兽,收集其双侧耳廓和外耳道的恙螨幼虫,用Hoyer's液封片后在显微镜下逐一分类鉴定到种.统计不同恙螨种类、构成比及其在对应寄生宿主的染螨率和螨指数,分析其在不同宿主体表和不同地域、生境的分布情况.结果 调查19个县(市)共采集到印度囊棒恙螨1267只,占采集到所有恙螨的1.36％;相对于云南省其它主要恙螨种,印度囊棒恙螨宿主特异性高,仅在7种3224只小兽体表有分布,且94.40％寄生在黄胸鼠体表.从地域分布来看,19个县(市)中6个县(市)有印度囊棒恙螨分布,主要集中在云南省南部和中西部.从生境来看,印度囊棒恙螨喜活动于坝区的房屋周围生境.结论 印度囊棒恙螨分布于云南省南部和中西部的坝区房屋周围生境,且集中寄生于黄胸鼠(恙虫病主要宿主动物)体表.     

Effect of Flavonoids in Morus indica on Blood Lipids and Glucose in Hyperlipidemia-diabetic Rats

Objective To investigate the effect and possible mechanism of flavonoids extracted from Morus indica(FMI) on blood lipids and glucose.Methods The experimental hyperlipidemia-diabetic rats were induced by high-fat diet(HFD) and low dose of Streptozotocin(STZ).Flavonoids-treated rats were pretreated with FMI(50,100,and 200 mg/kg).The plasma,skeletal muscle,and livers were isolated for biochemical assays,HE staining,immunohistochemistry,and Western blotting analysis.Results The results showed that the body weight in flavonoidstreated(100 and 200 mg/kg) rats was reduced(P < 0.05,0.01) compared to HFD-fed rats.FMI obviously reduced total cholesterol(P < 0.01),triglycerides(P < 0.05),and low-density lipoprotein cholesterol(P < 0.05),increased high-density lipoprotein(P < 0.05),and significantly decreased the atherosclerosis index(P < 0.01);FMI(100 and 200 mg/kg) also down-regulated the elevation of blood glucose induced by STZ(P < 0.05,0.01);At the meantime,FMI increased hepatic superoxide dismutase(SOD) activity and reduced hepatic malondialdehyde(MDA) content obviously.In addition,the results showed that the expression of hepatic CYP2E1 was markedly decreased while the expression of GLUT-4 in skeletal muscles was increased by FMI.Conclusion The above results demonstrate that the effect of FMI is related to its up-regulation of hepatic SOD activity,reduction of hepatic MDA content,down-regulation of hepatic CYP2E1 expression,and increase of GLUT-4 expression in skeletal muscle,which suggests that FMI may prevent or improve hyperlipidemia and hyperglycemia caused by an excessive HFD.     

Canna indica L. attenuates high-glucose- and lipopolysaccharide-induced inflammatory mediators in monocyte/macrophage

Ethnopharmacological relevance

Canna indica L. (CI) has been widely used as a folklore medicine in tropical and subtropical areas with beneficial effects in numerous diseases, including infection, rheumatism, hepatitis, and it has also been identified as an antioxidant.

Materials and methods

The present study aimed to investigate the effect of Canna indica CI ethanolic extract (CIE) on productions of nitric oxide (NO), prostaglandin E₂ (PGE₂), and interleukin-1β (IL-1β) in lipopolysaccharide (LPS)-induced RAW 264.7 macrophages. In addition, the effects of CIE in high glucose (HG)-induced U937 monocytes on mRNA expressions of IL-8 and monocyte chemoattractant protein-1 (MCP-1), and regulation of mitogen-activated protein kinase (MAPK) pathways were also identified.

Results

CIE was found to inhibit the production of inflammatory mediators including NO, IL-1β, and PGE₂ from LPS-induced RAW 264.7 macrophages. The increases in HG-induced mRNA expressions of IL-8 and MCP-1 were also significantly inhibited by CIE. Stimulation of HG in U937 monocytes resulted in activation of p38 MAPK, ERK1/2, and JNK. However, CIE treatment significantly decreased phosphorylation of p38 MAPK, ERK1/2, and JNK.

Conclusion

The present study demonstrated that CIE suppressed the LPS-induced inflammatory mediator production and also inhibited HG-induced inflammatory mediator expression by the regulation of MAPK pathway.     

Effect of Mangifera indica L. extract (QF808) on protein and hepatic microsome peroxidation.

The antioxidant activities of QF808, a steam bark extract of Mangifera indica L., were studied on hydroxyl-mediated oxidation of bovine serum albumin (BSA) and in a hepatic microsome system. The extract was effective in reducing the oxidation of BSA, since its half- maximal inhibition concentration (IC(50)) was 0.0049% w/v in the inhibition of carbonyl group formation and lower than 0.0025% w/v in the inhibition of sulfhydryl group loss. QF808 inhibited lipid peroxidation which was initiated enzymatically by reduced nicotinamide adenine dinucleotide phosphate (NADPH), IC(50)= 0.00075% w/v, or non-enzymatically by ascorbic acid, IC(50) = 0.0126% w/v. The extract tested did not inhibit NADPH-dependent cytochrome P-450 reductase activity, since it had no effect on the oxidation rate of NADPH. These results suggest that QF808 has an antioxidant activity, probably due to its ability to scavenge free radicals involved in microsome lipid peroxidation. In addition, QF808 antioxidant profile in vitro is probably similar to its principal polyphenolic component, mangiferin, a glycosylated xanthone.     

山莴苣染色体的核型分析

 目的　对山莴苣(Lactucaindica L.)染色体核型等进行研究,为该种鉴定、起源、演化、良种培育等的深入研究提供必要的细胞学资料。方法　采用常规制片方法 ,结合显微摄影技术对染色体进行检测分析。结果　山莴苣体细胞染色体数目2n=18;核型公式是K(2n)=18=4m+14sm,染色体相对长度组成为2n=18=8M₂+8M₁+2S,属于“3A”型。全组染色体总长是60.03μm,长臂总长40.33μm,核型不对称系数为67.18%。染色体总体积113.05μm³。结论　山莴苣染色体的数量、形态清晰,可为进一步的深入研究打下基础。     

了哥王不同提取部位抑菌作用研究

目的比较了哥王不同提取部位的体外抑菌作用。方法采用二倍稀释法测定不同提取物对11种细菌的最低抑茵浓度。结果乙酸乙酯提取物的抑菌效果显著强于正丁醇提取物，且两者对葡萄球菌属的细菌抑菌作用最强，水提取物基本没有抑菌作用。结论了哥王乙酸乙酯提取物抑菌效果显著，具有广谱抗菌作用。     

了哥王抗肿瘤活性部位筛选

目的:研究了哥王95%、75%、50%乙醇提取物、水提物及95%乙醇提取物的石油醚、氯仿、乙酸乙酯、正丁醇萃取部位对肿瘤细胞的增殖抑制作用,确定了哥王抗肿瘤活性部位。方法:采用四甲基偶氮唑盐(MTT)比色法考察了哥王不同提取物及95%乙醇提取物的不同溶剂萃取部位对Hela、SGC-7901、Bel-7402细胞的抗肿瘤活性。结果:了哥王95%乙醇提物对Hela、SGC-7901细胞有良好的抗肿瘤活性,其石油醚、氯仿、乙酸乙酯萃取部位对Hela、SGC-7901细胞均有不同程度的抗肿瘤活性。结论:石油醚、氯仿、乙酸乙酯萃取部位有较强的抗肿瘤活性,初步确定为了哥王抗肿瘤活性部位。     

红吹风的生药学鉴别

目的:对红吹风药材进行生药学鉴别。方法:分别对红吹风药材进行性状、显微及理化鉴别。结果:红吹风根的韧皮部有纤维束成群散在,木质部纤维束径向排列;茎中柱鞘纤维含大量草酸钙簇晶与针晶;叶中草酸钙簇晶多见,有外韧型维管束;理化鉴别提示有黄酮类成分。结论:以上特征可为红吹风药材的鉴别研究和开发利用提供参考依据。     

A new acylglycosyl sterol from quisqualis fructus

A new acylglycosyl sterol (4) was isolated from the MeOH extract of Quisqualis Fructus together with four known compounds. On the basis of spectroscopic data, their structures were elucidated as clerosterol (1), betulinic acid (2), methylursolate (3), 3-O-[6'-O-(8Z-octadecenoyl)-beta-D-glucopyranosyl]-clerosterol (4) and alpha-xylofuranosyluracil (5).