脑维康对D半-乳糖致脑老化模型大鼠学习记忆的影响

目的:观察脑维康(NWK)对D-半乳糖致脑老化大鼠模型学习记忆障碍的影响。方法:大鼠背颈部皮下连续注射D-半乳糖生理盐水(80 mg/kg)8周建立脑老化大鼠模型,灌胃给予NWK 8周。以Morris水迷宫试验检测模型大鼠的空间学习记忆能力,以分光光度法检测乙酰胆碱酯酶(acetylcholinesterase,AChE)、黄嘌呤氧化酶法测定过氧化物歧化酶(superoxide dismutase,SOD)、硫代巴比妥酸法测定丙二醛(maleic dialdehyde,MDA)的变化,以HE染色进行脑组织形态学观察。结果:D半-乳糖致脑老化大鼠在水迷宫中的游泳持续时间、路径长度明显延长。给药8周后,NWK 23 mg/kg、46 mg/kg组大鼠游泳持续时间、路径长度较模型组明显缩短,搜索策略均有改进。与空白组比较,模型组大鼠全脑AChE活力、MDA含量均明显升高,SOD活力明显降低。给药8周后,与模型组大鼠相比,NWK各给药组大鼠全脑AChE活力明显降低,NWK 46 mg/kg组大鼠全脑MDA含量明显降低,脑组织形态结构有所改善。结论:NWK可改善D-半乳糖致脑老化大鼠模型学习记忆能力。

针灸足三里穴对衰老模型小鼠皮肤中MDA、GSH-Px和Hyp的影响

目的观察了针灸足三里穴对衰老小鼠皮肤组织形态的影响。方法长期颈背部皮下注射D-半乳糖造成小鼠亚急性衰老模型,随机分为针刺组、艾灸组、模型组和空白组,检测皮肤组织中丙二醛(MDA)含量、谷胱甘肽过氧化物酶(GSH-Px)活力、羟脯氨酸(Hyp)含量。结果针灸足三里穴能够使衰老模型小鼠皮肤组织中的MDA含量减少,GSH-Px活力增强,Hyp含量增多。结论针灸足三里穴对小鼠皮肤衰老具有拮抗作用。

PROTECTIVE EFFECT OF TETRAMETHYLPYRAZINE ON LEARNING AND MEMORY FUNCTION IN D-GALACTOSE-LESIONED MICE

To explore the protective effect of tetramethylpyrazine (TMP) on the learning and memory function in D-galactose (D-gal)-lesioned mice. Methods C57BL/6 mice were injected (s.c.) 2% D-gal for 40 days (100 mg·kg-1·d-1). Normal saline, TMP, and Huper-zine A were respectively given by intragastric administration in different groups from the third week. Learning and memory ability was tested with Morris water maze for 5 days at the sixth week. After completion of behavioral test, the mice were sacrificed by decapitation. The brain was rapidly removed, and the cortex and hippocampus were separated. The superoxide dismutase (SOD) activity and malondialdehyde (MDA) content in the cortex were determined. At the same time, the activity of choline acetyltransferase (ChAT) and acetylcholinesterase (AChE), the binding sites (Bmax) and the affinity (KD) of M-cholinergic receptor in the cortex, and Bmax and KD of N-methyl-D-aspartate (NMDA) receptor in the hippocampus were determined. Results In this model group, (1) The deficit of learning and memory ability, (2) elevated MDA content and lowered SOD activity, (3) decreased AChE activity and M-cholinergic receptor binding sites in the cortex, and (4) lowered NMDA receptor binding sites were observed in the hippocampus, as compared with the normal control. TMP could markedly (1) attenuate cognitive dysfunction, (2) lower MDA content and elevate SOD activity, (3) increase the activity of ChAT and AChE, and M-cholinergic receptor binding sites in the cortex in the mice treated with D-gal. NMDA receptor binding sites were also increased in the hippocampus in the treated mice. Conclusion TMP can significantly strengthen antioxidative function, improve central cholinergic system function, protect NMDA receptor activity, and thus enhance the learning and memory ability in D-gal-lesioned mice.

姜黄素对D-半乳糖所致衰老小鼠学习记忆的影响

目的观察姜黄素对D半-乳糖所致衰老小鼠学习记忆障碍的保护作用。方法 50只ICR小鼠,随机分为5组:对照组,阿尔茨海默病(AD)模型组,姜黄素预处理组、同时处理组和后处理组。采用跳台试验和避暗试验方法,观察姜黄素对AD模型小鼠学习记忆障碍的影响。结果行为学试验显示,模型组小鼠潜伏期短,错误次数增多,与对照组比,P<0.05;姜黄素预处理组和同时处理组潜伏期延长,错误次数减少,学习记忆明显改善,与模型组比,P<0.05。结论姜黄素对AD模型小鼠的学习记忆能力减退具有改善作用。

Chemical Constituents from Ampelopsis grossedentata

Aim To study chemical constituents from Ampelopsis grossedentata. Methods Separation and purification were performed by using silica gel, polyamide, reverse-phase silica gel, Sephadex LH-20 column chromatographic techniques and silica gel PTLC. Structures were determined by means of physicochemical properties and spectral analysis. Results Four flavonoids were separated and identified from Ampelopsis grossedentata including dihydromyricetin (1), myricetin (2), myricitrin (3), and myricetin-3-O-β-D-galactopy...

Antiaging activity of low molecular weight peptide from Paphia undulate

Low molecular weight peptide (LMWP) was prepared from clam Paphia undulate and its antiaging effect on D-galactose-induced acute aging in rats, aged Kunming mice, ultraviolet-exposed rats, and thermally injured rats was investigated. P. undulate flesh was homogenized and digested using papain under optimal conditions, then subjected to Sephadex G-25 chromatography to isolate the LMWP. Administration of LMWP significantly reversed D-galactose-induced oxidative stress by increasing the activities of glutathione peroxidase (GPx) and catalase (CAT), and by decreasing the level of malondialdehyde (MDA). This process was accompanied by increased collagen synthesis. The LMWP prevented photoaging and promoted dermis recovery and remission of elastic fiber hyperplasia. Furthermore, treatment with the LMWP helped to regenerate elastic fibers and the collagen network, increased superoxide dismutase (SOD) in the serum and significantly decreased MDA. Thermal scald-induced inflammation and edema were also relieved by the LWMP, while wound healing in skin was promoted. These results suggest that the LMWP from P. undulate could serve as a new antiaging substance in cosmetics.

Antithrombin Ⅲ injection via the portal vein suppresses liver damage

AIM:To investigate the effects of antithrombin Ⅲ(AT Ⅲ) injection via the portal vein in acute liver failure.METHODS:Thirty rats were intraperitoneally challenged with lipopolysaccharide(LPS) and D-galactosamine(GalN) and divided into three groups:a control group;a group injected with AT Ⅲ via the tail vein;and a group injected with AT Ⅲ via the portal vein.AT Ⅲ(50 U/kg body weight) was administrated 1 h after challenge with LPS and GalN.Serum levels of inflammatory cytokines and fibrin degradation products,hepatic fibrin deposition,and hepatic mRNA expression of hypoxiarelated genes were analyzed.RESULTS:Serum levels of alanine aminotransferase,tumor necrosis factor-α and interleukin-6 decreased significantly following portal vein AT Ⅲ injection compared with tail vein injection,and control rats.Portal vein AT Ⅲ injection reduced liver cell destruction and decreased hepatic fibrin deposition.This treatment also significantly reduced hepatic mRNA expression of lactate dehydrogenase and heme oxygenase-1.CONCLUSION:A clinically acceptable dose of AT Ⅲ injection into the portal vein suppressed liver damage,probably through its enhanced anticoagulant and antiinflammatory activities.

LIPOPOLYSACCHARIDE－INDUCED CYTOTOXICITY AGAINST CULTURED MOUSE HEPATOCYTES AND THE ROLE OF NONPARENCHYMAL LIVER CELLS

Lipopolysaccharide (LPS) was found to induce significant hepatocytotoxicity against cultured mouse hepatocytes. Degeneration and necrosis of cultured hepatocytes and decrease of hepatocyte viability were prominent. The aspartate transferase level and 3H-TdR release in the medium were significantly increased after treatment, and the degree of these changes paralleled with LPS concentration. Various other parameters showed no significant difference between the hepatocytes cultured alone and those cocultured with nonparenchymal liver cells. However, if the nonparenchymal liver cells were isolated from mice which had been pretreated with D-galactosamine (GalN) not only was the hepatocyotoxicity induced by LPS enhanced, but the cells also showed certain cytotoxicity against cultured hepatocytes even without LPS, These results suggest that nonparenchymal liver cells might promote LPL-induced hepatocyte injury.

Combined administration of D-galactose and aluminium induces Alzheimer-like lesions in brain

Objective It has been reported that D-galactose （D-gal） can model subacute aging, and aluminum （AI） acts as a neurotoxin, but combined effects of them have not been reported. The present work aimed to reveal the effect of combined administration of D-gal and A1 in mice and compare the effect of D-gal treatment with that of A1 treatment. Meth- ods A1 was intragastricaHy administered and D-gal was subcutaneously injected into Kunming mice for 10 consecutive weeks. Learning and memory, eholinergic systems, as well as protein levels of amyloid β （Aβ） and hyperphosphorylated tau were determined using Morri water maze test, biochemical assays and immunohistochemical staining, respectively. Results The mice with combined treatment had obvious learning and memory deficits, and showed decreases in brain ace- tylcholine （ACh） level and in activities of choline acetyltransferase （CHAT） and acetyleholinesterase （ACHE）. Formation of senile plaque （SP）-like and neurofibrillary tangle （NFT）-like structures was also observed. The behavioral and pathologi- cal changes persisted for at least 6 weeks after withdrawal of D-gal and A1. Conclusion Combined use of D-gal and A1 is an effective way to establish the non-transgenic Alzheimer＇s disease （AD） animal model, and is useful for studies of AD pathogenesis and therapeutic evaluation.