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Objective To investigate the effects of S-allylcysteine ( SAC ) , on nitric oxide ( NO ) production and antioxidant enzyme activities in hyperlipidemic rats. Methods Male Wistar rats were randomly divided into seven groups. Five groups including normal control group ( normal diet) , model control group ( high-fat diet, HFD) and SAC low,medium,high treated group (high-fat diet +25,50,100 mg·kg-1 SAC) were sacrificed after 4 weeks dosing,while the other two groups including L-arginine group (normal diet+ 20 mg·kg-1 L-arginine) and SAC+L-arginine group (50 mg·kg-1 SAC+20 mg·kg-1 L-arginine) were sacrificed at 4 h after dosing. The serum, livers and kidneys were collected. The levels of NO, the activities of nitric oxide synthase ( NOS ) , antioxidant enzymes in vivo and L-arginine contents in serum were determined. Results Comparing with model control group, the activities of total NOS in serum and liver were significantly reduced in SAC-treated groups (P<0. 05). The level of L-arginine in SAC-treated groups was (8. 25 ± 1. 15), (7. 76 ± 1. 24) and (7. 22 ± 1. 64)μg·mL-1 , respectively. Compared with model control group, the level of L-arginine were significantly reduced in SAC-treated groups (P<0. 05). Comparing with L-arginine group, the activities of total NOS (T-NOS) and iNOS were reduced in SAC+L-arginine group. SAC treatment (100 mg·kg-1) significantly increased the activities of superoxide dismutase (SOD) (P<0. 01) and the level of glutathione (GSH) (P<0.01), and decreased the level of malondialdehyde (MDA) in serum and liver of hyperlipidemic rats. Conclusion These data suggest that SAC inhibits the NO production by reducing iNOS activity, arginine concentration and exhibited antioxidant activity, which may play a pharmacologically important role in protection from oxidative injury and pathogenesis of atherosclerosis.
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OBJECTIVE To observe the effect of baicalin on Aβ25-35 induced learning and memory deficits and changes in autophagy-related genes in mice so as to explore the related mechanisms of Alzheimer disease (AD) treatment . METHODS C57 mice were administered with 3μL Aβ25-35 3 mmol·L-1 by intracerebroventricular injection to establish an AD model. Baicalin was given by intracerebroventricular injection at the dose of 25, 50 and 100 mg · kg-1 for 15 d, respectively. The total distance and the central grid residence time were measured in the open-field test. The escape latency and the time to reach the platform were monitored in the Morris water maze trial. The autophagic vacuoles in the hippocampus of the mice were observed by transmission electron microscopy before the protein expressions of microtu?bule-associated protein 1 light chain 3 (LC3) and Beclin1 in brain tissue were analyzed by Western blot?ting assay. RESULTS Intracerebroventricular injection of Aβ25-35 could reduce the total distance from (3984±321)cm to (2790±306)cm and extend central grid residence time from (3.6±1.2)s to (8.8±2.9)s in the open-field test. The escape latency of water maze also increased from (22.0 ± 1.9)s to (38.8 ± 2.2)s. Autophagic vacuoles or late autophagic vacuoles and increased Beclin1 and LC3 and protein level were observed in the hippocampus after Aβ25-35 injection. Intraperitoneal injection of Baicalin 50 and 100 mg · kg-1 for fifteen consecutive days extended the total distance in open-field test to (3705 ± 337)cm and (3968 ± 448)cm, respectively, while the central grid residence time was reduced to (5.6 ± 1.8)s and (3.9±1.5)s, respectively. The total time taken to reach the platform in water maze test was reduced to (28.6± 1.9)s, (22.9 ± 1.7)s. Mitochondrial swelling, vacuolar membrane structure or autophagic vacuoles were visible in the hippocampus. LC3 and Beclin1 protein expression was significantly up-regulated(P<0.01). CONCLUSION Baicalin shows protective effect against Aβ25-35 induced learning and memory deficits, and this effect may be related to the activation of autophagy in the mouse hippocampus.
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Objective To investigate protective activity against Aβ25-35-induced cytotoxicity in PC12 cells of different extracts and ursolic acid, which were isolated from pyrola decorata. Methods Aβ25-35-induced cytotoxicity in PC12 cells was established as the model in vitro. The cultured PC12 cells were divided into blank control group, DMSO control group, model control group, different extract groups of pyrola decorate and ursolic acid(UA) group. The different extract groups included ether extract (PE), acetidin extract (AE), n-butanol extract (BE), the water extract (WE), 50% ethanol extract (HEE). MTT assay was used to test the optimum concentration, and the number of viable cells in culture medium was measured by ELISA at 490 nm wavelength. Results The cell viabilities in different extracts groups(PE, AE, BE, WE, HEE) were respectively 89.3%, 77.2%, 79. 2%, 75. 1% ,74. 0% at the concentration of 5. 0 mg ? mL-1 . Moreover, ursolic acid showed the best neuroprotective activity (88.9%) at the concentration of 500 μg?L-1 . Compared with model control group, the survival rate of each group was remarkably increased, and the protective activities of PE and UA were more significant among them. Conclusion Different polar extracts of pyrola decorata and isolated ursolic acid have neuroprotective effects on Aβ25-35-induced cytotoxicity in PC12 cells in certain degrees.
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AIM To investigate if inhibiting neutrophil infiltration and adhesion molecules expression is a part of the mechanisms of ginsenoside Rg1 protecting from cerebral injury after cerebral ischemia-reperfusion. METHODS Rats were pretreated with ginsenoside Rg1 25, 50 and 100 mg·kg-1·d-1, ig, for 7 d, respectively, then subjected to cerebral ischemia (middle cerebral artery occlusion) for 2 h and reperfusion for 22 h. The infarct volume and the neurological deficit were determined by TTC staining and Longa's scoring, respectively. The infiltration of neutrophils was evaluated by measuring the activity of myeloperoxidase (MPO). The expressions of intercellular adhesion molecule-1 (ICAM-1) and E-selectin were analyzed by Western blot. The permeability of the blood-brain barrier was evaluated by measurement of Evans blue content in brain tissue with spectrophotometer at 4 h after reperfusion. RESULTSCompared with vehicle-treated group, ginsenoside Rg1 (50 and 100 mg·kg-1·d-1) treatment significantly reduced infarct volume and elevated permeability of blood-brain barrier, alleviated the neurological deficit, and inhibited protein expressions of ICAM-1 and E-selectin in brain tissue. CONCLUSION Ginsenoside Rg1 has protective effects on cerebral injury induced by ischemia-reperfusion through inhibiting neutrophil infiltration and expression of the adhesion molecules.
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AIM To investigate if the beneficial effects of β-aescin on ischemia/reperfusion (I/R) induced cerebral injury are related to the inhibition of expressions of pro-inflammatory cytokines. METHODS Rats were pretreated ig with β-aescin for 7 d and then subjected to cerebral I/R injury induced by a middle cerebral artery occlusion. The infarct volume and the neurological deficit were determined by the method of TTC staining and the Longa's score. The permeability of the blood-brain barrier was evaluated by measurement of the Evans blue (EB)content in the brain with spectrophotometer. The serum contents of interleukin-8 (IL-8) and tumor necrosis factor-α(TNF-α) protein were determined by radioimmunoassay and ELISA assay. The expression of nuclear factor-κB (NF-κB) was evaluated with Western blot. RESULTS β-Aescin significantly reduced infarct volume (P<0.05 or P<0.01), ameliorated the neurological deficit and reduced the permeability of blood-brain barrier (P<0.05). Pretreated with β-aescin 30 and 60 mg·kg-1, the serum content of IL-8 and the expressions of TNF-α and NF-κB protein in brain tissue were significantly decreased (P<0.05). CONCLUSION β-Aescin has protective effects on cerebral injury through inhibiting the expression and release of the inflammatory mediators after I/R injury.
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The preliminary pharmacodynamic studies of the prepar ation of artificial Fel Serpentis and Bulbus Fritiliariae Cirrhosae and Shedan Chuanbei San (composed of natural Fel Serpentis and Bulbus Fri tiliariae Cirrhosae) were reported.The results showed that both of the above pre parations could prolong the cough latency and decrease cough frequeucies induced by ammonia within 3 min,promote the excretion of respiratory tract,increase the excretion of phenol red and inhibit auricular edema induced by xylol in mice. M eanwhile, the above two preparations could also inhibit Ach-induced tracheospasm in vitro.Therefore,the replacement of natural Fel Serpentis with the artificial in the preparation of Shedan Chuanbei San is reasonable.
ABSTRACT
The preliminary pharmacodynamic studies of the preparation of artificial Fel Serpentis and Bulbus Fritiliariae Cirrhosae and Shedan Chuanbei San (composed of natural Fel Serpentis and Bulbus Fritiliariae Cirrhosae) were reported.The results showed that both of the above preparations could prolong the cough latency and decrease cough frequeucies induced by ammonia within 3 min,promote the excretion of respiratory tract,increase the excretion of phenol red and inhibit auricular edema induced by xylol in mice. Meanwhile, the above two preparations could also inhibit Ach-induced tracheospasm in vitro.Therefore,the replacement of natural Fel Serpentis with the artificial in the preparation of Shedan Chuanbei San is reasonable.