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Objective To compare the dissolution curves of metronidazole tablets from 38 national manufactures and original drugs of Britain in four dissolution mediums,and provide the reference for the quality and clinical effect consistency evaluation of metronidazole tablets.Methods Paddle method was adopted at 50 r · min-1 in four dissolution mediums with the volume of 900 mL.The dissolution profiles were determined by ultraviolet spectrophotometry.The cumulative dissolution percentages were calculated and the dissolution curves were drawn.Similarity factor (f2)was used for comparing of the differences between dissolution curves.Results The dissolution profiles of 4 manufactures in pH 1.2 and 9 manufactures in pH 4.5 were similar (f2 ≥ 50)to that of original drugs,only 1 and 3 were similar to original drugs in water and pH 6.8,respectively.There are no companies whose dissolution curve were similar to that of original drugs in 4 dissolution mediums.Conclusion Great difference exists between domestic manufactures and pharmaceutical enterprises of origin in dissolution behaviors of metronidazole tablets.In order to ensure the consistency between the metronidazole tablets generics and original drugs of Britain in quality and clinical effect.It is advisable for the relevant companies to improve their product quality by improving the formulation and preparation.
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Objective To investigate the effect of Exendin-4 (Ex-4) on ischemia/reperfusion (I/R) injury-induced apoptosis in primary rat cortical neurons and the possible underlying mechanisms.Methods Rat cortical neurons were cultured in vitro,identified by NES-immunohistological staining and immunofluorescence staining,and randomly divided into the following groups: control group,I/R group and Ex-4 group.RT-PCR was performed to establish the existence of active glucagon-like peptide-1 receptor (GLP-1R).ELISA was used to measure the neuronal cytoplasmic cAMP level. MTT was used to detect viability. Fluorescent DNA binding dye Hoechest 33258 was used to reveal apoptosis. C/EBP-homologous protein (CHOP) and growth arrest and DNA-damage-inducible gene 34 (GADD34) mRNAs were detected by real-time PCR. Results The apoptosis rate induced by ischemia 6 h/reperfusion 12 h was 77.0% ±5.3% and was decreased to 27.0% ± 3.5% after Ex-4 ( 0. 4 μg/ml ) treating ( t = 19. 462,P ＜ 0. 01 ).Levels of CHOP and GADD34 mRNA in cortical neurons increased since 4 h and peaked at 12 h after reperfusion. Ex-4 group showed a sharp elevation of levels of CHOP and GADD34 mRNA,peaking at 8 h reperfusion,and then tended to decrease.Conclusions Ex-4 has protective effect against rat cortical neurons injury induced by ischemia/reperfusion. The protective effect may be related to inhibition of ESR-related neuron apoptosis via regulation of unfolded protein response.
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Objective To observe the effects of passive movement on the functional outcome after occlusion of the middle artery in the brain and reperfusion, and to explore the molecular mechanisms involved. Methods Cerebral infarction models were established in rats using left middle cerebral artery occlusion ( MCAO). The survivors were randomly divided into a passive movement group and a natural recovery group. There was also a sham-operated group and a normal group. Passive movement treatment (twice a day, twenty min per time) was started at different times after reperfusion. The expression of brain-derived neurotrophic factor (BDNF) and B cell lymphoma/leukemia-2 gene (Bcl-2) were determined using real-time PCRs. Results Expression of BDNF and Bcl-2 was detected a-round the infarction area in both groups. The expression of BDNF and Bcl-2 was highest in the sub-groups where passive movement was begun 24 or 48 h after the operation. Conclusions The expression of BDNF and Bcl-2 in the brain peaks when daily, moderate intensity passive movement is administered beginning 24 to 48 h after reperfusion. Passive movement might have a protective and rehabilitative effect after cerebral infarction.
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Objective To study the effect of electroacupuncture (EA) combined with transcranial magnetic stimulation (TMS) on the expression of the B-cell lymphoma/leukemia-2 gene (Bcl-2) and brain derived neurotrophic factor (BDNF) after cerebral infarction. Methods One hundred Sprague-Dawley rats were randomly and equally divided into a normal group, a sham-operated control group, a model group and an EA plus TMS group. A cerebral infarction model was established in the latter two groups using left middle cerebral artery occlusion (MCAO). Five-member subgroups of the EA plus TMS group were then treated at 6, 12, 24,48 and 72 hours after reperfusion. Sham EA plus TMS was given to similar sub-groups from the other groups at the same time points. The expression of Bcl-2 mRNA and BDNF mRNA were measured using a RT-PCR at the 14th day. Results Positive expression of Bcl-2 mRNA and BDNF mRNA was detected around the infarction in all groups. The average expression of both was significantly higher in the EA plus TMS group than in the model group. Bcl-2 mRNA peaked when the therapy was administered at 24 hours and BDNF mRNA at 48 hours.Conclusions The expression of Bcl-2 mRNA and BDNF mRNA is maximized when EA plus TMS is administered 24-48 hours after cerebral infarction. EA plus TMS does have protective and rehabilitative effects on rats after cerebral infarction.
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Objective To study the effect of transcranial magnetic stimulation (TMS) on the rehabilitation of rats with cerebral infarction. Methods One hundred Sprague-Dawley rats were randomly divided into a normal group, a sham-operated control group, a model group and a TMS group with 25 rats in each group. A cerebral infarction model was established in the latter two groups by left middle cerebral artery occlusion (MCAO). TMS was started at either 12 or 24 hours after reperfusion, and sham-TMS was given to the first two groups at the same time points. The expression of Bcl-2 mRNA and BDNF mRNA were measured by RT-PCR after 14 days. Results Bcl-2 mRNA and BDNF mRNA were detected in all groups. The expression of Bcl-2 mRNA in the TMS-12 h group, and that of BDNF mRNA in the TMS-24 h group were significantly higher than in the other groups. Conclusions The expression of Bcl-2 mRNA and BDNF mRNA in the brains of rats after cerebral infarction peak when TMS is administered 12 h and 24 h after reperfusion, respectively. TMS might have protective and rehabilitative effects on rats after cere-bral infarct.