Effect of Saffron Extract, Astaxanthin, and Carnosic Acid on the Levels of Matrix Metalloproteinase-9 and on Body Weight Changes in Arthritis Experiments

The aim of this study was to explore the potential effect of natural compounds and their combination with methotrexate (M) on levels of matrix metalloproteinase-9 (MMP-9) as a key biochemical parameter in rat adjuvant arthritis. Further change of body weight was selected as one of clinical parameters monitored in this animal model

Effect of high-fat-fructose diet on synaptic plasticity in hippocampus and lipid profile of blood serum of rat: pharmacological possibilities of affecting risk factors

The aim of this study was to determine pharmacological possibilities of influencing the risk factors of metabolic syndrome (MetS). Hypertriacylglycerolemic (HTG) rats fed with high-fat-fructose diet (HFFD) were used as a model of the MetS. Wistar rats fed with standard diet were used as negative control group. HTG rats fed with HFFD for 8 weeks were used as positive control group. The effects of atorvastatin and SMe1EC2 were tested. The compounds were administered to the HTG rats after 5 weeks of HFFD, once a day for 3 weeks. After 8 weeks, the blood serum lipid profile and electrophysiology of neurotransmission in hippocampal sections were evaluated in vitro. SMe1EC2 and atorvastatin had a significant effect on total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-cholesterol) and atorvastatin had a significant effect on triacylglycerols (TGs). SMe1EC2 improved the long-term potentiation (LTP) course in the hippocampus

Hippocampal electrophysiological responses and changes in oxidative stress marker and serum lipid profile to pharmacological and non-pharmacological treatments of high-fat-fructose diet induced metabolic syndrome

The aim of our study was to evaluate the possibility of influencing the risk factors of metabolic syndrome (MetS) and metabolic cognitive syndrome. As a model of MetS, we used high-fat-fructose diet (HFFD) fed hypertriacylglycerolemic (HTG) rats. Control group included HTG rats fed with HFFD during 8 weeks (HFFD8). Furthermore, we tested the effect of pharmacological and non-pharmacological therapies. Non-pharmacological therapy, which we chose, was a change in diet from HFFD (5 weeks) to standard one (3 weeks) and thus caloric restriction (HFFD5+3). The drug we used was rosmarinic acid (RA; 100mg/kg), which we administered to rats after 5 weeks of HFFD once a day for consecutive 3 weeks with current change in diet to standard one (HFFD5+3+RA) or during lasting last 3 weeks of HFFD (HFFD8+RA). After 8 weeks of experiment, lipid peroxidation markers, lipid profile of blood serum, and neuronal transmission and synaptic plasticity (long-term potentiation [LTP]) in hippocampal sections were evaluated in vitro. We observed a significant effect of dietary change in lipid profile (decreased total cholesterol and low-density lipoprotein cholesterol [LDL-cholesterol] and increased high-density lipoprotein cholesterol [HDL-cholesterol]). The combination of pharmacological and non-pharmacological treatments caused a decrease in total cholesterol, LDL-cholesterol, and lipid peroxidation in blood serum. Change in HFFD to standard diet without treatment resulted in slight improvement in neuronal transmission in the hippocampus and caloric restriction alone also had positive effect on LTP maintenance. Our results suggest that combination of pharmacological and non-pharmacological approaches had better impact on the biochemical parameters of MetS in blood serum, but weak impact on neuronal functions in the hippocampus, where the expected positive effect was achieved only by caloric restriction