Validity of silver, chitosan, and curcumin nanoparticles as anti-Giardia agents

This study was carried out to evaluate the anti parasitic potential of silver, chitosan, and curcumin nanoparticles as anti-Giardia agents. Non-treated infected control rats were inoculated with Giardia lamblia cysts in a dose of 2?×?10(5) cysts/rat. Experimental group was infected then treated with curcumin, curcumin nanoparticles, chitosan, chitosan nanoparticles, and silver nanoparticles as single or combined therapy. The number of Giardia cysts in stools and trophozoites in intestinal sections were detected. Toxicity of nanoparticles was evaluated by comparing hematological and histopathological parameters of the normal control group and treated non-infected control group. The amount of silver was also measured in the liver, kidney, small intestine, lung, and brain of rats treated with silver nanoparticles. The number of the parasites in stool and small intestinal sections decreased in treated infected rats compared with infected non-treated ones. The effect in the single therapy was better with nanoparticles, and the best effect was detected in nano-silver. The combined therapy gave better results than single. Combination between nanoparticles was better than the combination of nano-forms and native chitosan and curcumin. The best effect was detected in combinations of nano-silver and nano-chitosan but with no full eradication. In conclusion, the highest effect and complete cure was gained by combining the three nano-forms. The parasite was successfully eradicated from stool and intestine. None of the treatments exhibited any toxicity. Accumulated silver in different organs was within the safe limits.     

Investigation of brain-derived neurotrophic factor (BDNF) gene expression in hypothalamus of obese rats: Modulation by omega-3 fatty acids

Purpose: The aim of this study was investigating the effect of omega-3 fatty acids (ω-3 FAs) on brain-derived neurotrophic factor (BDNF) gene expression, using in vivo and in vitro models, to unravel the potential mechanisms of polyunsaturated fatty acids use in obesity.

Materials and methods: Twenty-nine Sprague-Dawley rats were divided into three groups; lean controls fed normal chow diet for 14 weeks, obese controls fed 60% of their diet as saturated fats for 14 weeks, and ω-3 FAs-treated rats fed 60% saturated fat diet for 14 weeks with concomitant oral administration of 400?mg/kg/day ω-3 FAs, mainly docosahexaenoic acid and EPA, from week 12 to week 14. For the in vitro experiment, hypothalamic cells from six obese rats were cultured in the presence of different concentrations of ω-3 FAs to determine its direct effect on BDNF expression.

Results: In vivo results showed that obesity has negative effect on BDNF gene expression in rat hypothalamus that was reversed by administration of ω-3 FAs. Obese rats showed hypercholesterolemia, hypertriglyceridemia, normoinsulinemia, hyperglycemia and hyperleptinemia. Treatment with ω-3 FAs showed significant decrease in serum total cholesterol and TAG. Also serum glucose level and HOMA index were decreased significantly. In vitro results demonstrated the increase in BDNF expression by ω-3 FAs in a dose-dependent manner.

Conclusions: Obesity causes down-regulation of BDNF gene expression that can be reversed by ω-3 FAs treatment, making them an interesting treatment approach for obesity and metabolic disease.     

Exacerbation by nicotine of the cyclosporine A-induced impairment of beta-adrenoceptor-mediated renal vasodilation in rats

Nicotine is implicated in smoking-related renovascular impairment and worsening of existing nephropathies. In the present study, we investigated whether nicotine aggravates the deleterious effect of the immunosuppressant drug cyclosporine A (CsA) on renal vasodilation induced by the beta-adrenoceptor agonist isoprenaline. Bolus isoprenaline (0.03-8.0 micromol) elicited dose-dependent vasodilation of phenylephrine-preconstricted perfused kidneys that was attenuated by infusion at 5 mL/min of nicotine (5 x 10(-4) mol/L) or CsA (2 micromol/L). Further, chronic administration of nicotine (0.4 mg/kg per day) or CsA (20 mg/kg per day) for 3 weeks reduced isoprenaline-induced vasodilation and elevated plasma urea and creatinine concentrations, effects that were magnified when both nicotine and CsA were administered concurrently. The role of endothelial and smooth muscle signalling in the acute nicotine/CsA renovascular interaction was investigated. Vasodilation caused by 0.25 micromol isoprenaline was attenuated by 6 micromol/L propranolol and 10 mmol/L tetraethylammonium (TEA), potentiated by 100 micromol/L hexamethonium and 7 micromol/L diclophenac, and virtually abolished in 80 mmol/L KCl-preconstricted tissues. N(G)-Nitro-L-arginine (L-NNA; 200 micromol/L), methylene blue (10 micromol/L), 3-[(3-cholamidopropyl)-dimethyl-ammonio]-1-propane-sulphonate (CHAPS; 0.2% for 30 s), nifedipine (750 nmol/L), atropine (1 micromol/L) and SQ22536 (an adenylyl cyclase inhibitor; 3 x 10(-5) mol/L) had no effect on isoprenaline responses. Nicotine (5 x 10(-4) mol/L) reduced isoprenaline-induced vasodilation and this effect was potentiated by concurrent CsA (2 micromol/L) infusion. Nicotine-induced impairment of the vasodilator response to isoprenaline was reduced by hexamethonium and potentiated by L-NNA, methylene blue, CHAPS and nifedipine. Alternatively, CsA exacerbation of the nicotine-isoprenaline interaction was abolished by propranolol, L-NNA, methylene blue, CHAPS, L-arginine, TEA and nifedipine. 5. In summary, nicotine and CsA produce additive impairment of kidney function and beta-adrenoceptor-mediated renovascular control, nitric oxide (NO)-cGMP signalling tonically restrains nicotine-induced impairment of isoprenaline vasodilation and the endothelial NO-K+ pathway modulates the aggravating effect of CsA on nicotine-isoprenaline interactions.     

Preparation and distribution of 5-fluorouracil 125I sodium alginate-bovine serum albumin nanoparticles

ＮＴＲＯＤＵＣＴＩＯＮＮａｎｏｐａｒｔｉｃｌｅ（ＮＰ）ｉｓａｎｃｏｌｏｉｄａｌｄｉｓｐｅｒｓｉｏｎｓｙｓｔｅｍ,ｗｉｔｈｄｉａｍｅｔｅｒｓｒａｎｇｉｎｇｆｒｏｍ１０ｎｍｔｏ１０００ｎｍ．Ｔｈｅｐａｒｔｉｃｌｅｓｅｘｉｓｔｍａｉｎｌｙｉｎｔｈｅｏｒｇａ...     

赤芝子实体中灵芝酸类成分的研究

自赤芝［Ｇａｎｏｄｅｒｍａｌｕｃｉｄｕｍ（Ｆｒ．）Ｋａｒｓｔ．］子实体的二氯甲烷提取物中分离得到一个新的四环三萜化合物，命名为灵芝酸ＤＭ（ｇａｎｏｄｅｒｉｃａｃｉｄＤＭ，Ｉ）。根据光谱（ＵＶ，ＩＲ，１ＨＮＭＲ，１３ＣＮＭＲ，ＭＳ２ＤＮＭＲ）分析，确定其结构为Ｉ式。同时还分离得到二个已知的灵芝酸类化合物，即灵芝酸Ａ（ｇａｎｏｄｅｒｉｃａｃｉｄＡ，Ｉ）和灵芝酸Ｃ（ｇａｎｏｄｅｒｉｃａｃｉｄＣ，ＩＩ）。     

防治成人呼吸窘迫综合征的人工重组肺泡表面活性剂研制II.生物发光法筛选制剂处方

在前期用表面化学方法进行防治成人呼吸窘迫综合征的药物制剂处方筛选基础上,通过建立尘肺动物模型,用生物发光技术从清除自由基能力角度对制剂进行处方筛选,获到了有良好表面性能和一定自由基清除能力的人工重组肺泡表面活性剂制剂处方。该制剂有待经模型动物防治试验评价。     

中药材龟板和鳖甲中DNA的提取与扩增

中药材龟板和鳖甲中ＤＮＡ的提取与扩增王亚明，周开亚，吴平，徐珞珊（南京师范大学生物系，南京２１００９７；中国药科大学生药学研究室，南京２１０００９）龟鳖类药材在我国使用历史悠久，具补阴益气的功效。《中国药典》（１９９０年版）规定龟甲（龟板）的原动物为...     

无环鸟苷亲脂性前体药物脂质体的制备及体外抗病毒活性(英文)

本文通过将无环鸟苷(acyclovir,简称ACV)2’位羟基分别与月桂酰氯或棕榈酰氯进行酯化反应,制得亲脂性前体药物无环鸟苷月桂酸酯和无环鸟苷棕榈酸酯(分别简称为C_(12)-ACV和C_(16)-ACV),使脂质体包封率从ACV的29.9％提高到C_(12)-ACV的95.6％和C_(16)-ACV的97.1％;漏泄实验表明在4℃透析60h后,一半以上的ACV从脂质体中漏泄,而C_(12)-ACV和C_(16)-ACV的滞留率分别为70％和80％;体外抗疱疹病毒的试验中,在最低试验浓度0.044μmol/L时,ACV不显示抗病毒活性,而C_(16)-ACV脂质体抑制细胞病变率达75％,说明前体药物通过与脂质体脂膜的结合增加了药物的进入细胞能力,从而提高了ACV的抗病毒能力。