| For the past few years, study show that chronic inflammation become the important one changes of pathology and physiology, hypercholesterolemia, hypertension, diabetes mellitus, smoking like these CHD risk factors, can damage the endothelial cell of the artery, the changes of structure and function in the endothelial cell make immune cell adhesion towards to endothelial cell or under the endothelial cell, swallowing modified LDL becoming foam cells slowly, smooth muscle cell proliferate, atherosclerosis take place early. To study and research physiological and pathological mechanism of atherosclerosis, to prevent beforehand and to treat atherosclerosis earlier becomes the hot of research in the cardiovascular diseases. We utilized the model detective techniques, such as serology, immunohistochemistry and optical microscope, radioimmunology etc. The paper observes the effect of the treatment of HXJZL, and surveys the changes of artery atherosclerosis inflammation in rats from aspects of blood pressure, blood fat, endothelium constriction and relation factor, inflammation marker, inflammation-damage signal transduction, so that we can master more precisely data information by this and newer thread and method of treating CHD utilizing compound recipe Chinese medicine.Objective: To study the protective effects and mechanism of HXJZL on artery atherosclerosis inflammation early.Methods: 60 healthy male Wister rats were fed one week adaptability, the feeding room is constant temperature, the temperature is 22±2℃, humidity of the room is 40-60%, we provide the rats from enough clearing water and sunshine about 12 hours later, the rats were randomly divided into groups namely blank group, model group, Cardboard group, simvastatin group, HXJZLH group, HXJZJLL group every group has 12 rats. The rats of bank group model group, HXJZLH group, HXJZLL group rats feed with animal feeds 12 weeks which is made of lots of fat. On the fourth week, the four groups'rats were injected Vd3 by 700 thousand U/kg in peritoneal cavity. The injection was finished in three days so that artery atherosclerosis model can complete smoothly, the bank group and model group were fed with physiological saline by 10ml/d/kg, simvastatin group fed with simvastatin liquid (=10 times clinical dose). HXJZL high dose and low dose group were given HXJZL at the dose of 45g/d/kg (equal to 20 times to clinical dose) and 22.5g/d/kg (equal to 10 times to clinical dose) weight, medicinal broth's CO were 4.5g/ml and 2.25g/ml.The time of intragastric administration last 8 weeks. (Dosage under the 'one human body surface area ratio method in rats' dosage conversion rats, converts dosage of rats, human body weight calculated according to 60 kg ). At the late of medication, all groups stop feeding about 12 hours .In the morning, all groups rats were anaesthetized by urethane of 25% (0.5ml/100g), blood pressure were measured in the common carotid artery, later, the rats were killed and the sera were collect to determine the TC, TG, LDL, HDL, NO, ET-1, HE staining was employed to analyze the pathological damage in aortic arch, immunohistochemisty method detect to PKC ELLISA detect to C reactive protein.Results:1. Blood pressureCompared to the Systolic pressure of rats, Systolic blood pressure of rats in model group decreased significantly, the difference was statistical significance (P < 0.01), compared with the model group, statins group of systolic blood pressure decreased, difference is statistically significant (P < 0.01), compared with the simvastatin group, Systolic blood pressure of rats in HXJZL high dose group did not decease, difference is not statistically significant (P > 0.05), compared with the simvastatin group, HXJZLL group did not decease obviously(P < 0.01) .2 lipid changeCompared with Blank group, the content of TG, TC, LDL in Model group increased obviously, HDL decreased, the difference was statistical significance (P < 0.01). Compared with Model group, the content of TG, TC, LDL in Simvastatin group, HXJZL High, Low group all decreased obviously, HDL increased obviously, the difference was statistical significance (P < 0.01). Compared with Simvastatin group, the content of TC in HXJZLH group increased, the difference was statistical significance (P < 0.01), TG, HDL, LDL no difference (P > 0.05), the content of TC, LDL in HXJZLL group increased, HDL decreased, the difference was statistical significance (P < 0.01), while TG was no difference (P > 0.05). Compared with Simvastatin group, the content of TC in HXJZLHigh group increased obviously, the difference was statistical significance (P < 0.01), TG, HDL, LDL no difference (p > 0.05); the content of TC, LDL in HXJZLLow group increased, HDL decreased, the difference was statistical significance (P < 0.05), while TG was no difference (p > 0.05).3 Changes of Serum nitric oxide (NO) and endothelin (ET-1).Compared with Blank group, the level of NO among the model group decreased obviously(P < 0.01). Compared with the blank group ,the levels of Simvastatin group, HXJZLH group and HXJZLL group increased obviously(P < 0.01), there are no statistically significant during the HXJZLH group and Simvastatin group (P > 0.05).Compared with Blank group, the level of ET-1 among the model decreased significantly (P < 0.01), compared the blank group, levels of ET-1 of other three group increased significantly (P < 0.01). There are no statistically significant during the HXJZLH group and Simvastatin group (P > 0.05). Compared with HXJZLL group ,level of ET-1 of Simvastatin group deceased (P < 0.01). Compared with HXJZLL group level of ET-1 of HXJZLH group decreased (P < 0.05).4 Histopathological injuriesBlank control group there was no obvious injury, such as inflammation of the pathological changes, Model group in the membrane and intimal were thickening, we can see a lot of Macrophages, monocyte infiltration, proliferation, accompanied by patchy, punctate calcification and foam cell formation during the Intimal and medial artery. Outer layer of fibroblast proliferate, structural disorder due to complete. Simvastatin group did not proliferate in the membrane and intimal, haves not Inflammatory cell infiltrating and proliferating, however, the structural disorder due to complete. HXJZL high dose group on each floor for the structure of the thoracic aorta wall is clear, there is a slight thickening of intimal layer Middle-substantial fibroblasts proliferate, but the structure is complete. HXZJL low-dose group have a slight thickening in thoracic aortic intima. Smooth muscle cells in the middle is less tidy, there is a small amount of fibrous tissue hyperplasia, Substantial outer layer of fibroblasts, structural integrity is unclear.5 Expression of PKCCompared with the blank group, expression of PKC of Rats of model group was significantly strong (P < 0.01), Compared with model group, the treatment group, the expression of PKC of the treatment groups have different degrees of reduced, expression of PKC of simvastatin group and HXJZL high-dose group is Significantly less, it is no statistical difference between the two (P > 0.05), PKC of HXJZL low-dose group have a certain extent expression. Compared with the model group, PKC expression of HXJZLL group is decreased (P < 0.01).6 The expression of CRPCompared with the blank group, CRP levels of model group were significantly elevated in rats (P < 0.01). Compared with model group, CRP of the treatment groups were lower than model group, there is significant difference (P < 0.01), simvastatin and HXJZL high-dose group was no significant difference in CRP levels (P > 0.05), compared with the simvastatin group ,HXJZL low dose group in CRP levels increased, there is significant difference (P < 0.01).Conclusion: HXJZL have a protective effect at early atherosclerotic inflammatory injury in rats and can reduce systolic blood pressure, regulate the balance of ET/NO, Inhibiting the PKC activity, reducing the level of C-reactive protein, blocking the development of inflammatory injury. |
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