BACKGROUND: The content of aluminium generally increases in the cerebral cells of patients with senile dementia. Aluminium poisoning in brain has inner link with senile dementia. Naloxone is the specific antagonist of opioid receptor, which can be applied in the treatment of senile dementia according to foreign reports.OBJECTIVE: To investigate protective effects of naloxone on aluminium trichloride-induced memory impairment of senescence-accelerated mice and its mechanism.DESIGN: Randomized controlled trial.SETTING: Jilin Medical College.MATERIALS: The experiment was completed in Laboratory of Pharmacology of Jilin Medical College (formerly the Jilin Military Medical College) from February 2001 to February 2003. A total of 100 healthy adult Kunming mice were selected and randomly divided into 5 groups: control group, model group, naloxone 0.1 mg/kg group, naloxone 0.3 mg/kg group and naloxone 0.9 mg/kg group, with 20 in each group. Except the control group, subcutaneous injection with 70 mg/kg aluminium trichloride was given to the mouse in each group once a day for continuous 7 days; besides this, intraperitoneal injection with 0.1, 0.3, 0.9 mg/kg naloxone was given to the mouse in naloxone groups and the same amount of physiological saline was given to the mouse in the control group.METHODS: The methods of jumping stand and escaping dark were conducted to detect learning ability and memory of mice. Meanwhile, the content of malondialdhehyde in liver and mono-amine oxidase B in brain of mice were also detect.MAIN OUTCOME MEASURES: ① Results of jumping stand experiment of aluminium trichloride-induced model of senescence. ② Results of escaping dark experiment of aluminium trichloride-induced model of senescence. ③ Comparison of malondialdhehyde and mono-amine oxidase B among each group.RESULTS: ① Results of jumping stand experiment of aluminium trichloride-induced model of senescence: Compared withmodel group, the frequency of electric shocks suffered by aluminium trichloride mice and the amount of suffered animals within 5 minutes significantly decreased in control group and naloxone 0.1, 0.3, 0.9 mg/kg groups. The experiment was repeated 24 hours later, naloxone could significantly prolong the latency of the mouse jumping down from the platform for the first time (P ＜ 0.01).Meanwhile, naloxone could decrease the amount and the frequency of mist&es of aluminium trichloride mouse within 3 minutes (P ＜ 0.01). ② Results of escaping dark experiment of aluminium trichloride-induced model of senescence: Compared with model group, the latency of aluminium trichloride mouse entering dark box was significantly prolonged and the frequency of electric shocks suffered by aluminium trichloride mice obviously increased in control group and naloxone 0.1, 0.3, 0.9 mg/kg groups (P＜0.01). ③ Comparison of malondialdhehyde and mono-amine oxidase B among each group: Malondialdhehyde was more in model group than in naloxone groups (P＜0.01). Mono-amine oxidase B was more in model group than in the other groups (P＜0.01).CONCLUSION: Naloxone has protective effects on aluminium trichlorideinduced memory impairment of senescence-accelerated mice, which can improve learning ability and memory. The mechanism is probably relevant to the effects of decrease of mono-amine oxidase B and elimination of lipid peroxide.

Objective To investigate the effect of procyanidin from Vaccinium vitisidaea on the proli-feration of cardiac fibroblast(CFb) induced by angiotensin Ⅱ(AngⅡ),and to explore its mechanism.Methods The CFb proliferation of cultured neonatal rat was induced by AngⅡ and detected by MTT assay.The levels of collagen Ⅰ,collagen Ⅲ,and TGF-?1 were measured by ELISA.The change of NO content and iNOS activity were measured by nitric acid reductase method and spectrophotometry.Cell cycle was assessed via flow cytometry(FCM). The expression of cell cycle regulatory protein p27 was determined by the combination of immunocytochemical staining and image analysis software.Results CFb Proliferation,collagen content,and TGF-?1 levels in culture medium were markedly inhibited when CFb were treated with procyanidin at concentration of 25,50,and 100 mg/L(P

Aim To explore the effect of Procyanidin from Vaccinium(PC) on the myocardial fibrosis and its mechanism.Methods The model of myocardial fibrosis in rats was built by subcutaneous injection of isoprenaline(Iso) for 5 mg?kg-1?d-1 in vivo.Meanwhile,rats were treated with PC 100,200 and 400 mg?kg-1?d-1 by gastrointestinal administration.The contents of hydroxyproline(Hyp),malondialdehyde(MDA) and the activity of superoxide dismutase(SOD) in left ventricle were assayed with spectrophotometry respectively.Changes of myocardial ultrastructure were observed by electronic microscope.The cultured neonatal rat CFb was isolated by trypsin digestion method.The proliferation of CFb was induced by Angiotensin Ⅱ and assessed by thiazolyl blue(MTT) assay.PC was added in different dosage(25,50 and 100 mmol?L-1).Ⅰ,Ⅲ collagen quantification and TGF-?1 levels were determined by the ELISA.Results In vivo,compared with model group,the contents of hydroxyproline and malondialdehyde of left ventricle were significantly reduced and the activity of superoxide dismutasein left ventricle was markedly enhanced in PC three groups(P

OBJECTIVETo detect the effect and mechanism of procyanidin foom vaccinium (PC) on myocardial fibrosis in rats.

METHODThe myocardial fibrosis model in rats was built by subcutaneous injection of 5 mg x kg(-1) x d(-1) of isoprenaline (Iso) for 7 days in vivo while intragastrically administrating PC 100, 200 and 400 mg x kg(-1) x d(-1) for 14 days. Following the model was established, myocardial indexes (heart weight/body weight, HW/BW and left ventricalar weight/body weight, LVW/BW) were measured. Besides, angiotensin II and I , III collagen quantification levels in blood serum were determined respectively by ELISA. The change in the content of nitric oxide (NO) in blood serum was determined with colorimetry. The content of malondialdehyde (MDA) in left ventricle was assayed with spectrophotometry. The contents of lactate dehydrogenase (LDH) and creatine kinase (CK) in blood serum were detected with automatic biochemistry analyzer.

RESULTCompared with the control group, the myocardial indexes, the contents of I , III collagen quantification, angiotensin II in blood serum and malondialdehyde in left ventricle were markedly increased and the content of nitric oxide in blood serum was decreased, the contents of lactate dehydrogenase and creatine kinase in blood serum were markedly increased in Iso model group (P<0.05 or P<0.01). Compared with the model group, the myocardial indexes were decreased, the contents of I , III collagen quantification, angiotensin II in blood serum were reduced in PC 200 and 400 mg x kg(-1) x d(-1) groups (P<0.05 or P<0.01). The content of nitric oxide in blood serum was increased, the content of malondialdehyde in left ventricle was markedly decreased, the contents of lactate dehydrogenase and creatine kinase in blood serum were markedly decreased in PC three groups (P<0.05 or P<0.01).

CONCLUSIONPC could inhibit collagen synthesis by decreasing angiotensin II level and increasing the content of nitric oxide and antioxidation, and thereby inhibiting myocardial fibrosis and protect myocardium in rats.

Angiotensins ; blood ; Animals ; Antioxidants ; administration & dosage ; pharmacology ; Biflavonoids ; administration & dosage ; pharmacology ; Catechin ; administration & dosage ; pharmacology ; Endomyocardial Fibrosis ; chemically induced ; drug therapy ; metabolism ; Female ; Isoproterenol ; adverse effects ; Male ; Malondialdehyde ; metabolism ; Nitric Oxide ; blood ; Proanthocyanidins ; administration & dosage ; pharmacology ; Rats ; Rats, Wistar ; Vaccinium ; chemistry ; Ventricular Remodeling ; drug effects