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BACKGROUND:Many animal experiments and clinical observation proved that dispeling turbid phlegm herb has good adjustment function on serum lipid, lipoprotein and liver lipid. OBJECTIVE: To observe the effects of dispeling turbid phlegm herb on monocyte chemotactic factor-1, C-reactive protein and serum lipids in rabbits with dietary atherosclerosis. METHODS: A total of 50 New Zealand white rabbits were randomly divided into five groups. Rabbits in the blank control group were fed with basic feed, and simultaneously intragastricaly administrated physiological saline 10 mL/kg per day, for 10 consecutive weeks. Rabbits in the model group were given high-fat diet to prepare atherosclerosis models, and simultaneously intragastricaly administrated physiological saline 10 mL/kg per day, for 10 consecutive weeks. Rabbits in the phlegm turbidity treatment group were given high-fat diet to prepare atherosclerosis models, and simultaneously intragastricaly administrated dispeling turbid phlegm herb 10 mL/kg per day, for 10 consecutive weeks. Rabbits in theXuezhikang group were given high-fat diet to prepare atherosclerosis models, and simultaneously administratedXuezhikang 10 mL/kg per day, for 10 consecutive days. Rabbits in the phlegm turbidity treatment group were given high-fat diet for 10 weeks to prepare atherosclerosis models, and intragastricaly administered physiological saline 10 mL/kg per day for 6 weeks, and then given dispeling turbid phlegm herb 10 mL/kg per day for 4 weeks. At 10 weeks, serum lipid, C-reactive protein, and monocyte chemokine 1 mRNA expressions were detected, and pathological observation of the aorta was performed. RESULTS AND CONCLUSION:Xuezhikang and dispeling turbid phlegm herb could decrease serum total cholesterol, triglyceride, low density lipoprotein cholesterol, high density lipid protein cholesterol, C-reactive protein and monocyte chemokine 1 mRNA expression level, and apparently inhibited atherosclerotic changes. The preventive effect of dispeling turbid phlegm herb was better that its therapeutic effect.
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[ ABSTRACT] AIM:To investigate the effect of polysaccharide from Fructus corni ( PFC) on cardiomyocytes against hypoxia/reoxygenation ( H/R) injury and its possible relationship with ROS/PKC/p38 MAPK pathway.METHODS:Prima-ry cardiomyocytes were isolated from neonatal SD rats and randomly divided into normal group, H/R group, PFC (20 mg/L, 100 mg/L and 200 mg/L) preconditioning+H/R groups, chelerythrine+PFC (100 mg/L)+H/R group and SB203580+PFC (100 mg/L)+H/R group.The cell viability was measured by inverted microscopic observation.Apoptosis in the car-diomyocytes was detected by Hoechst 33258 staining and fluorescence microscopy.The levels of lactate dehydrogenase ( LDH) and superoxide dismutase ( SOD) in the cell culture supernatants, and the reactive oxygen species ( ROS) in the cells were also measured by microplate reader.The protein levels of PKC, p-p38 MAPK and HSP70 in the cells were detec-ted by Western blotting.RESULTS:Compared with normal group, the cell viability and beating frequency were decreased in H/R group.LDH and ROS contents, apoptotic rate and p-p38 MAPK level increased significantly (P<0.01).Compared with H/R group, PFC preconditioning increased beating frequency, SOD activity and the protein level of PKC and HSP70, and decreased ROS production, the protein level of p-p38 MAPK and cell apoptotic rate.However, the effect of PFC was in-hibited by chelerythrine or SB203580.CONCLUSION:PFC may protect cardiomyocytes from hypoxia/reoxygenation injury. Its mechanism is possibly involved in the inhibition of ROS via increasing the activity of SOD and the activation of PKC, and suppression of excessive activation of p38 MAPK.
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Objective To evaluate the role of protein kinase C (PKC ) in reduction of mitochondrial injury during myocardial ischemia-reperfusion (I/R) by ischemic preconditioning in rats .Methods Forty male Sprague-Dawley rats ,aged 12-13 weeks ,weighing 280-320 g ,were randomly divided into 4 groups ( n=10 each) using a random number table:sham operation group (S group) ,I/R group ,ischemic preconditioning group (IP group) and PKC inhibitor chelerythrine group (C group) .Myocardial I/R was produced by 35 min occlusion of left anterior descending branch of coronary artery followed by 120 min reperfusion .Ischemic preconditioning was induced by 3 episodes of 5 min occlusion of left anterior descending branch at 5 min intervals before myocardial ischemia . Chelerythrine 1 mg/kg was injected intravenously via the caudal vein before ischemic preconditioning in group C . At 120 min of reperfusion ,the animals were sacrificed and the hearts were immediately removed .Mitochondrial suspension was prepared for determination of activities of succinate dehydrogenase (SDH ) , xanthine oxidase (XOD ) , glutathione peroxidase (GSH-Px ) and Ca2+-ATPase , content of Ca2+ , myocardial mitochonerial permeability transition pore (mPTP) opening and membrane potential (Δψm ) .Results Compared with S group , the activities of XOD and Ca2+-ATPase ,content of Ca2+ and mPTP opening were significantly increased ,and the activities of SDH and GSH-Px and Δψm were decreased in I/R group ( P<0.05) .Compared with I/R group ,the activities of XOD and Ca2+-ATPase , content of Ca2+ and mPTP opening were significantly decreased , and the activities of SDH and GSH-Px and Δψm were increased in IP group ( P<0.05) .Compared with IP group ,the activities of XOD and Ca2+-ATPase , content of Ca2+ and mPTP opening were significantly increased , and the activities of SDH and GSH-Px and Δψm were decreased in C group ( P<0.05) .Conclusion PKC is involved in reduction of mitochondrial injury during myocardial I/R by ischemic preconditioning in rats .
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We found previously that water soluble extract of Liriope spicata Lour (SanMaiDong) possesses cardioprotective action. The paper reported that effects of total aminoacid ex- traded from Liriope spicata Lour (Tal) on experimental myocardial ischemia in rats. The results indicate that Tal (5 mg?kg-1 ,ip) obviously antagonized ischemic ECG changes induced by pituitrin in rats. In myocardial ischemic rats caused by isoprenaline (8 mg?kg-1) Tal 15 mg? kg-1ip significantly reduced ST and decreased CPK release and lowered the content of MDA. In a myocardial ischemic mode) induced by ligat-ing the left anterior descending coronary artery in rats, Tal 15 mg?kg-1ip remarkably decreased plasma CPK and FFA levels and was found todiminish the infarct size. The ratio of its infarct size (5. 80%) is similar to that of propranolol (5. 41%),but apparently smaller than that of ligated group (18.55%). The results suggest that Tal can protect ischemic myocardium and this action may relate to the prevention of my-ocardial lipid peroxication and improvement of myocardial metabolism.