Effect of levocarnitine on TIMP-1,ICAM-1 expression of rats with coronary heart disease and its myocardial protection effect

Objective:To study the effect of levocarnitine(L-CN) on tissue inhibitor of metalloproteinase-1(TIMP-1) and intercellular adhesion molecule-1(ICAM-1) expression of rats with coronary heart disease and evaluate the protective effect of L-CN on myocardial cells.Methods:Highfat diet feeding and intraperitoneal injection of pituitrin was performed on rats in model group and CHD Model of rats was built.Rats with successful model-building were selected and divided into L-CN group and Ctrl group randomly.Rats in L-CN group were given L-CN treatment,with intraperitoneal injection of 200 mg·kg^(-1)?d^(-1) and successive administration for 3 d.Rats in Ctrl group were given equal volumes of normal saline.Blood was collected from carotid artery at different time and expression quantity of creatine kinase-MB(CK-MB) and Troponin Ⅰ(Tn Ⅰ)in serum was detected.Rats in each group were put to death and were separated to obtain the myocardial tissue.Real-time PCR and Western Blotting hybridization were performed to detect the TIMP-1.ICAM-1 expression in myocardial tissue in each group.Statistical analysis was employed to explore the expression changes of TIMP-1 and ICAM-1.and ELISA test was used lo analyse the expression changes of myocardial necrosis marker- CK-MB and Tn I to learn the effect of L-CN and its myocardial protective effect.Results:The total cholesterol,triglyceride and blood glucose levels of rats in model group were significantly higher than that in control group,which indicated that due to high-fat diet feeding,blood lipid of rats in model group was obviously higher than that in control group.In myocardial tissue of rats in model group,TIMP-I level significantly reduced and ICAM-1 level significantly increased(P<0.0l).In model group,after L-CN treatment.TTMP-I level had double increase,while ICAM-1 level had 43%of decrease in L-CN group compared with Ctrl group.After L-CN intervention treatment.CK-MB and Tn Ⅰ content in L-CN group relatively reduced compared with Ctrl group.The difference among groups was obvious(P<0.01).Condusions:L-CN could increase the TTMP-I expression level and inhibit the ICAM-1 expression level.L-CN has a certain myocardial protective

The effect of Levocarnitine on nutritional status and lipid metabolism during long-term maintenance hemodialysis

Objective To investigate the effect of Levocarnitine on lipid metabolism and nutritional status of maintenance hemodialysis(MHD)patients and possible mechanism.Methods A total of 40 MHD patients [mean age(53.5±7.1)years] who underwent normal hemodialysis more than 6 months were randomly classified into two groups,Levocarnitine supplemented group(LS-G)(n=20;Levocarnitine supplementation after each normal hemodialysis session,at a dose of 1.0 g/day by intravenous administration)and control group(C-G)(n=20;normal hemodialysis).Before treatment,one month and three months after treatment we respectively measured or observed the following items,the tolerance to hemodialysis,carnitine level in plasma,C-reactive protein,IL-6,TNF-α,percentage of neutrophil,and some relevant nutritional parameters,such as lipid profile,transferrin,total protein,albumin and prealbumin levels.Comparative analysis was conducted between the two groups.Results In LS-G three months after treatment,the levels of carnitine,hemoglobin,and prealbumin in plasma were significantly increased(P<0.05),but C-reactive protein,neutrophil percentage,low-density lipoprotein and triglyceride were significantly decreased(P<0.05)in contrast to those in C-G and before treatment.Transferrin,total protein,and albumin were elevated in LS-G,with no statistical significance.Conclusion There was a significant improvement of lipid metabolism and nutritional status for the long-term maintenance hemodialysis patients with Levocarnitine supplementation.And this improvement is related to the decrease of inflammatory factors.

Effect of levocarnitine+coenzyme Q10 adjuvant therapy on vasoactive molecules,endothelial injury and oxidative stress in patients with chronic heart failure

Objective: To study the effect of levocarnitine + coenzyme Q10 adjuvant therapy on vasoactive molecules, endothelial injury and oxidative stress in patients with chronic heart failure. Methods: A total of 90 patients with chronic heart failure who were treated in the hospital between December 2014 and December 2016 were collected and divided into control group and observation group by random number table method, 45 cases in each group. Control group received conventional therapy, and observation group received levocarnitine + coenzyme Q10 adjuvant therapy on the basis of conventional therapy. The differences in vasoactive molecule, endothelial injury and oxidative stress levels were compared between the two groups before and after treatment. Results: Before treatment, the differences in vasoactive molecule, endothelial injury and oxidative stress levels were not statistically significant between the two groups of patients. After treatment, serum vasoactive molecules ET-1, AngⅡ and TXB2 contents of observation group were lower than those of control group while NO content was higher than that of control group;endothelial function indexes FMD level was higher than that of control group;serum oxidative stress indexes SOD and T-AOC contents were higher than those of control group while MDA and ROS contents were lower than those of control group. Conclusion: Levocarnitine + coenzyme Q10 adjuvant therapy can optimize the vascular activity, and reduce the endothelial injury and systemic oxidative stress response in patients with chronic heart failure.

Effect of adjuvant levocarnitine therapy on EPO resistance, oxidative stress response and inflammatory response in patients with hemodialysis

Objective: To study the effect of adjuvant levocarnitine therapy on EPO resistance, oxidative stress response and inflammatory response in patients with hemodialysis. Methods: A total of 78 patients who received maintenance hemodialysis in Beijing Chaoyang District Shuangqiao Hospital between May 2015 and October 2016 were selected and randomly divided into two groups, the levocarnitine group received levocarnitine combined with conventional anemia correction therapy, and the control group accepted routine anemia correction therapy. The extent of EPO resistance, oxidative stress response and inflammatory response in two groups of patients were assessed before treatment as well as 3 months and 6 months after treatment. Results: 3 months and 6 months after treatment, the rhuEPO dosage and ERI, Nrf-2 , ARE, HO-1 and NQO-1 expression in peripheral blood mononuclear cells as well as AOPP, 8-OHdG, MDA, MCP-1, sICAM-1, PTX3, IL-4 and IL-10 levels in serum of levocarnitine group had been gradually decreasing while the rhuEPO dosage and ERI, Nrf-2, ARE, HO-1 and NQO-1 expression in peripheral blood mononuclear cells as well as AOPP, 8-OHdG, MDA, MCP-1, sICAM-1, PTX3, IL-4 and IL-10 levels in serum of control group were without significant change. Conclusion: Adjuvant levocarnitine therapy can significantly improve the EPO resistance, oxidative stress response and inflammatory response in patients with hemodialysis.

Altered Mental Status and Hyperammonemia after Overdose of Valproic Acid with Therapeutic Valproic Acid Concentrations

Valproic acid is used in the treatment of multiple disorders. Adverse effects from valproic acid include hepatotoxicity, hypotension, metabolic acidosis, and decreased mental status. Valproic acid also causes hyperammonemia. Many physicians assume that this is due to a supratherapeutic valproic acid concentration;when in fact, it can occur with therapeutic valproic acid concentrations. This is because the hyperammonemia may be related to carnitine deficiency and disruption of the urea cycle, which can both occur with therapeutic valproic acid concentrations. We report a patient presented to the emergency department with alteration of mental status after ingesting valproic acid for recreational purposes, who developed hyperammonemia with a therapeutic valproic acid concentration.