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Depression after myocardial infarction is closely related to the theory of ascending and descending of qi and blood. The core pathogenesis is analyzed as disorder of qi and blood, mental damage, uncontrolled upward and downward movement, and pivot movement failure. The treatment method is to regulate qi and blood, invigorate qi and activate blood circulation and restore the rise and fall of visceral qi. Nourishing qi and promoting blood circulation should invigorate qi in the first. Appropriate blood activating drugs should be selected according to the degree of blood stasis, so that the blood circulation is smooth and the spirit has dependence. The key to restoring the normal balance of qi movement of visceral organs is to regulate not only liver ascending and lung descending but also spleen. Clinicians need pay attention to the nature of drug lifting and falling, conforming the physiological functions of the organs, to restore the rising and falling of the qi movement of internal organs.
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Objective To evaluate the effect of nimodipine pretreatment on postoperative cognitive function in diabetic rats. Methods One hundred and eighty healthy male Wistar rats, aged 3-4 months, weighing 260-310 g, were divided into 6 groups ( n=30 each) using a random number table method: op-eration group ( O group) , diabetes mellitus group ( DM group) , diabetic cognitive impairment group ( DCI group) , nimodipine plus operation group ( N+O group) , nimodipine plus diabetes mellitus group ( N+DM group) and nimodipine plus diabetic cognitive impairment group ( N+DCI group) . Diabetes mellitus model was established by intraperitoneal injection of streptozotocin 55 mg∕kg. Nimodipine 1 mg∕kg was intraperito-neally injected at 6 weeks after establishing the model in DCI and N+DCI groups and at 2 weeks after estab-lishing the model in DM and N+DM groups, and laparotomy was performed under sevoflurane anesthesia at 30 min after the end of administration. Morris water maze test was performed at 1 day before operation and 3 and 7 days after operation. Then rats were sacrificed, and hippocampal tissues were taken for determination of the apoptotic rate of neurons, cytoplasmic calcium concentrations ( by flow cytometry) and expression of caspase-3 in hippocampus ( by Western blot) . Results Compared with the baseline at 1 day before opera-tion, the escape latency was significantly prolonged, the number of crossing the original platform was re-duced, the apoptotic rate of hippocampal neurons and cytosolic calcium concentrations were increased, and the expression of caspase-3 was up-regulated at each time point after operation in six groups ( P<0. 05 ) . Compared with group O, the escape latency was significantly prolonged, the number of crossing the original platform was reduced, the apoptotic rate of hippocampal neurons and cytosolic calcium concentrations were increased, and the expression of caspase-3 was up-regulated at each time point after operation in DM and DCI groups ( P<0. 05) . The escape latency was significantly shortened, the number of crossing the original platform was increased, the apoptotic rate of hippocampal neurons and cytosolic calcium concentrations were decreased, and the expression of caspase-3 was down-regulated at each time point after operation in group N+DM as compared with group DM and in group N+DCI as compared with group DCI ( P<0. 05) . Conclu-sion Nimodipine pretreatment can improve postoperative cognitive function in diabetic rats, and the mech-anism may be related to inhibiting calcium overload-induced apoptosis in neurons.
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OBJECTIVE: To study the anti-gout effect of aqueous extract from the stems and leaves of Erythropalum scandens (ASLE). METHODS: The mice were randomly divided into normal group, model group, allopurinol group (positive control, 5 mg/kg), ASLE low-dose, medium-dose and high-dose groups (1 300, 2 600, 5 200 mg/kg, by raw material; similarity hereinafter), with 10 mice in each group. Except for normal group, other groups were given potassium oxonate intragastrically to induce hyperuricemia model. One hour after modeling, normal group and model group were given constant volume of normal saline intragastrically; administration group was given relevant medicine intragastrically, once a day, for consecutive 7 d. One hour after last administration, the levels of serum uric acid (SUA) and serum creatinine (Scr) were detected by colorimetry assay. Another mice were randomly divided into normal group, model group, indomethacin group (positive control, 7.5 mg/kg), ASLE low-dose, medium-dose and high-dose groups, with 10 mice in each group. Normal group and model group were given constant volume of normal saline intragastrically; administration group was given relevant medicine intragastrically, once a day, for consecutive 7 d. After last administration, except for normal group, the mice were given sodium microcrystalline urate via toes to induce gouty arthritis model. Before and 1, 2, 4, 6, 8 h after modeling, the circumference of the same part of the inflamed limbs and toes of mice in each group was measured by wire binding method, and the degree of toe swelling was calculated. The number of white blood cell (WBC), neutrophil (NEU) and lymphocyte (LYM) were detected by animal hematology analyzer. The levels of SUA and Scr were measured by colorimetry assay. The content of NO in toe tissue was determined by Griess method. RESULTS: The experimental results of hyperuricemia model showed that the levels of SUA and Scr in mice were significantly higher in model group than those in normal group (P<0.01). Compared with model group, above indexes of mice were decreased significantly in administration group (P<0.05 or P<0.01). The experimental results of gouty arthritis model showed that the level of SUA, the degree of toe swelling (2-8 h), the number of WBC, NEU and LYM, NO content in model group were increased significantly, compared with normal group (P<0.05 or P<0.01). Compared with model group, the levels of SUA and Scr (ASLE groups), the degree of toe swelling [indomethacin group, ASLE high-dose group (2-8 h), ASLE low-dose group (2, 6 h), ASLE medium-dose group (6 h)], the number of WBC and NEU (administration groups), the number of LYM (indomethacin group) and NO content (administration groups except for ASLE low-dose group) were decreased significantly in administration groups (P<0.05 or P<0.01). CONCLUSIONS: The anti-gout effect of ASLE may be associated with promoting uric acid metabolism, anti-inflammatory and improving renal function.
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<p><b>OBJECTIVE</b>To investigate the protective effect of sesamin against cadmium chloride (CdCl2)-induced cardiotoxicity in rats.</p><p><b>METHODS</b>Fifty male Wistar rats were randomly assigned to five groups: control group, CdCl2 group, and low-, middle-, and high-dose sesamin groups. The control group was given normal saline. The CdCl2 group and sesamin groups were intraperitoneally injected with CdCl2 (5 mg/kg×2 d), and the low-, middle-, and high-dose sesamin groups were given 20, 40, and 80 mg/kg sesamin, respectively. All treatments lasted for four weeks. ECG was measured by a physiological recorder, and serum myocardial enzyme levels were determined by biochemical assay. The heart was weighed, and heart tissues were used in histopathological examination and determination of malondialdehyde (MDA) level.</p><p><b>RESULTS</b>Compared with the control group, the CdCl2 group showed significantly higher levels of serum CK and CK-MB, an increased heart coefficient, significant ST-segment elevation, and higher level of MDA in myocardial tissue (P < 0.05). Histopathological analysis showed edema of myocardial tissues and cells, myocardial fibers disorder, karyopyknosis, and uneven or deep staining of nuclear chromatin. Different doses of sesamin relieved the myocardial pathological changes induced by CdCl2, and high-dose sesamin was the most effective. The middle- and high-dose sesamin groups showed significantly reduced serum CK and CK-MB levels compared with the CdCl2 group (P < 0.05). The heart coefficient of the high-dose sesamin group (0.19±0.01%) was significantly lower than that of the CdCl2 group (0.21±0.01%) (P < 0.05). Myocardial MDA levels of the three sesamin groups (42.32±4.65, 36.71±5.34, and 33.12±4.62 nmol/mg pro, respectively) were all significantly lower than that of the CdCl2 group (55.87±3.65 nmol/mg pro) (P < 0.05).</p><p><b>CONCLUSION</b>Sesamin can relieve myocardial injury induced by CdCl2, and one possible mechanism is the enhancement of antioxidant capacity of myocardial tissue.</p>
Subject(s)
Animals , Male , Rats , Cadmium Chloride , Toxicity , Creatine Kinase, MB Form , Blood , Dioxoles , Pharmacology , Heart , Lignans , Pharmacology , Malondialdehyde , Metabolism , Myocardium , Metabolism , Pathology , Rats, WistarABSTRACT
Objective To evaluate the effects of sevoflurane preconditioning on postoperative cognitive dysfunction in aged rats.Methods One hundred and twenty healthy male Sprague-Dawley rats,aged 18 months,weighing 400-450 g,were randomly divided into 3 groups (n =40 each) using a random number table:control group (group C),operation group (group O),and sevoflurane preconditioning group (group Sev).In group C,the rats were only anesthetized with pentobarbital sodium and did not undergo operation.In group O,the rats were anesthetized with pentobarbital sodium and underwent 30 min of exploratory laparotomy.In group Sev,the rats inhaled 2.4% sevoflurane for 30 min and then inhaled air for 30 min,and the other procedures were similar to those previously described in group O.At 30 min before operation and on 1st,3rd,5th and 7th days after operation,Morris water maze test was performed to record the escape latency,time of staying at the original platform quadrant and frequency of crossing the original platform.At 30 min before operation and on 1st and 7th days after operation,10 rats in each group were sacrificed and hippocampi were isolated to detect the apoptotic rate and intracellular [Ca2 +] i (using flow cytometry) and the ultrastructure of hippocampal neurons was observed with transmission electron microscope.Results Compared with group C,the escape latency was significantly prolonged,the time of staying at the original platform quadrant was shortened,the frequency of crossing the original platform was decreased,and the apoptotic rate and intracellular [Ca2 +] i were increased after operation in O and Sev groups (P <0.05).Compared with group O,the escape latency was significantly shorten,the time of staying at the original platform quadrant was prolonged,the frequency of crossing the original platform was increased,and the apoptotic rate and intracellular [Ca2+]i were decreased after operation in group Sev (P < 0.05).Microscopic examination showed no abnormality in the ultrastructure of hippocampal neurons in group C,and the pathological changes of the ultrastructure of hippocampal neurons were obvious in group O,and were significantly attenuated in group Sev.Conclusion 2.4% sevoflurane preconditioning can reduce postoperative cognitive dysfunction in aged rats,and regulation of imbalance of calcium homeostasis and reduction of cell apoptosis are involved in the mechanism.