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Fenofibrate is a common lipid-lowing drug activating peroxisome proliferator-activated receptor alpha (PPRAα).Recent studies have found that fenofibrate possesses anticancer properties.Its specific mechanisms include inhibiting cell metabolism and formation of new tumor vessels,arresting cell circle,weakening cell motility,and inducing cell apoptosis.Those properties are partly independent of PPRAα.Due to its low side-effects,it's hopefully to be used as an anticancer adjuvant drug.
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ObjectiveTo assess the efficacy of adjuvant therapy with fenofibrate for primary biliary cirrhosis (PBC). MethodsCNKI, Wanfang Data, China Biology Medicine, PubMed, Embase, and Cochrane library were searched for the pertinent literature of randomized controlled trials (RCTs) of adjuvant therapy with fenofibrate for PBC published up to December 31, 2014. Data extraction and quality assessment were carried out, and the data were statistically analyzed by Stata10.1 software. Respectively, for heterogeneity test. The fixed effect model is chosen for homogeneity, and the random effect model is chosen for heterogeneity. ResultsSix RCTs met the inclusion criteria. Treatment with fenofibrate was associated with significantly reduced levels of gamma-glutamyl transpeptidase, alanine aminotransferase, and alkaline phosphatase in PBC patients (SMD=-1.595, -0.447, and -2.125, respectively, all P＜0.05). There were no significant changes in the levels of aspartate aminotransferase and total bilirubin after adjuvant therapy with fenofibrate (both P＞0.05). Also, fenofibrate led to no significant improvement in immunoglobulin M (P＞0.05). ConclusionFenofibrate, which improves the indicators of liver function but leads to no changes in immunological indicators, appears to be an effective adjuvant therapy in PBC patients. There is a critical need for more large-scale, multi-center, high-quality RCTs to determine its effect on liver disease-related morbidity and mortality.
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ObjectiveTo assess the efficacy of adjuvant therapy with fenofibrate for primary biliary cirrhosis (PBC). MethodsCNKI, Wanfang Data, China Biology Medicine, PubMed, Embase, and Cochrane library were searched for the pertinent literature of randomized controlled trials (RCTs) of adjuvant therapy with fenofibrate for PBC published up to December 31, 2014. Data extraction and quality assessment were carried out, and the data were statistically analyzed by Stata10.1 software. Respectively, for heterogeneity test. The fixed effect model is chosen for homogeneity, and the random effect model is chosen for heterogeneity. ResultsSix RCTs met the inclusion criteria. Treatment with fenofibrate was associated with significantly reduced levels of gamma-glutamyl transpeptidase, alanine aminotransferase, and alkaline phosphatase in PBC patients (SMD=-1.595, -0.447, and -2.125, respectively, all P＜0.05). There were no significant changes in the levels of aspartate aminotransferase and total bilirubin after adjuvant therapy with fenofibrate (both P＞0.05). Also, fenofibrate led to no significant improvement in immunoglobulin M (P＞0.05). ConclusionFenofibrate, which improves the indicators of liver function but leads to no changes in immunological indicators, appears to be an effective adjuvant therapy in PBC patients. There is a critical need for more large-scale, multi-center, high-quality RCTs to determine its effect on liver disease-related morbidity and mortality.
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Objective To investigate the changes of NF-κB p65, IL-6 and cell apoptosis in sec-ondary brain injury after traumatic brain injury and the influence of fenofibrate on these parameters in rats. Methods Ninety-eight male Sprague-Dawley ( SD) rats were randomly divided into two groups:fenofibrate group ( n =49) and control group ( n =49) .The fenofibrate group was induced with the improved Feeney method and received intragastrica of lipanthyl 60 mg/(kg? d) immediately after injury.The control group were received intragastrica of sodium chloride injection 2 ml/( kg? d) immediately after injury and twice everyday until rats were killed.Each group was divided into seven subgroups by sacrificed time after injury, those were 1 h, 3 h, 6 h, 12 h, 24 h, 3 d, and 7 d, and each subgroup got 7 rats.Each subgroup was ran-domly selected three rats after being killed to detect expressions of NF-κB p65 and IL-6 of rat contusion peri tissues brain tissues with immunohistochemical method.While using terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling ( TUNEL) method was used to observe the peri cell apoptosis after brain contusion.Results The expressions of NF-κB p65 and the IL-6 in each fenofibrate group were significantly decreased relative to the control group ( P <0.05),and a significant positive correlation between both pa-rameters in two groups ( P <0.01) .At the same time, the number of apoptotic cells was decreased ( P <0.05).Conclusions Fenofibrate was probably through the route of relieving inflammation response to re-duce the change of secondary brain injury after traumatic brain injury and decrease neural cell apoptosis, and then provide protection of neurocytes.
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Thirty six patients with hypertriglyceridemia and impaired glucose regulation or newly diagnosed type 2 diabetes, whose fasting plasma glucose was ≤8.0 mmol/L, were treated by fenofibrate for 3 months. Lipid profile, insulin during intravenous glucose tolerance test and oral glucose tolerance test ( including glucose) were measured before and after treatment After treatment, lipid profile was significantly improved. Insulinogenic index (△I30/△G30) and acute insulin response were significantly increased (98. 9vs. 129. 2, 3558.9 vs. 4783. 3 pmol · L - 1 · min - 1, respectively, P ＜ 0. 05 ). Fasting insulin and insulin resistant index in homeostasis model assessment ( HOMA IR) decreased ( 128. 6 vs. 84. 8 pmol/L, 4. 8 vs.3.0, respectively, P ＜0. 05 ). The improvement of insulin secretory function was more significant in patients with higher triglyceride (TG ＞ 3. 3 mmol/L). These results indicate that short-term lipid-lowering treatment with fenofibrate can improve β-cell function and insulin resistance. Patients with higher triglyceride are likely to achieve more benefit from lipid-lowering treatment.
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Objective To examine the effects and mechanisms of simvastatin and fenofibrate, and combination of the two drugs on the expression of apolipoprotein M (apoM). Methods The male C57BL/6N mice ( n =32) were random divided into four groups, including control group (with no special treatment), statin group (with simvastatin [10mg/( kg · d) for 4 weeks], fibrate group (with fenofibrate [100mg/( kg · d) for 4 weeks] and combination group ( with simvastatin [10mg/( kg· d)] and fenofibrate [100mg/( kg · d) for 4 weeks]. The levels of apoMmRNA and protein, hepatic nuclear factor (HNF-1α)mRNA, liver X receptor-α (LXRα) mRNA in mouse liver were measured. Results Both of simvastatin and fenofibrate can increase the expression of apolipoprotein M ( 1.97 ± 0. 04,2. 02 ± 0. 02 ) and HNF-1αmRNA ( 1.74 ± 0. 05,1.71 ± 0. 04). Combination group obtained more effects than either single agent ( P ＜ 0. 05 ). Simvastatin could decrease the expression of LXRα mRNA ( 1.00 ± 0. 02 ) ( P ＜ 0. 05 ). Fenofibrate could increase the expression of LXRα mRNA(2. 80 ±0. 04) ( P ＜0. 05). No significant difference in LXRα expression was seen between combination( 1.56 ±0. 03 ) and control group( 1.53 ±0. 03 )( P ＞0. 05). Conclusions Simvastatin and fenofibrate can increase apoM expression. Treatment with combination of the two drugs is more effective, and the mechanism might be related to the regulation of HNF-1α and LXRα.
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Objective: To explore the exact role of ghrelin in glyco-and lipo-metabolism.Methods: We compared the levels of ghrelin mRNA in gastric tissue,ghrelin in gastric tissue and plasma among LETO rats(non diabetes,n=10),OLETF rats(type 2 diabetes,n=10),OLETF/M rats(OLETF rats managed with Metformin at the dose of 100 mg/kg weight,n=10) and OLETF/F rats(OLETF rats managed with Fenofibrate at the dose of 20 mg/kg weight,n=10).The levels of ghrelin mRNA were tested by Northern blotting,and the ghrelin content in gastric tissue and plasma detected by RIA.Results: At the age of 30 weeks,the ghrelin fasting plasma levels of OLETF rats were lower than those of LETO rats(37.49?6.42 vs 58.52?5.85,P0.05).However,the fasting blood plasma ghrelin levels of OLETF/F group were more than those that of the untreated OLETF rats(62.02?7.35 vs 37.49?6.42,P
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Objective To observe the effects of fenofibrate on the expression of scavenger receptor class B type I(SRBI) in adipose tissue and adipocytes of hypercholesterolemia rabbits.Methods Ten male New Zealand white rabbits were fed with high cholesterol diet for 8 weeks,and were randomly divided into two groups: high cholesterol group and treatment group.The rabbits in the high cholesterol group were maintained cholesterol diet for 4 weeks and those of the treatment group were fed with the same cholesterol diet supplemented with fenofibrate(30 mg/kg/day) for 4 weeks.Five rabbits in control group were fed with normal diet for 12 weeks.Subcutaneous adipose was collected for adipocytes culture.The expressions of SRBI mRNA in adipose tissue and adipocytes were evaluated by semi-quantitative reverse transcription-polymerase chain reaction(RT-PCR).Results The serum levels of total cholesterol and low density lipoprotein cholesterol were significantly higher in the high cholesterol group and treatment group than those of the control group(P0.05).The expressions of SRBI mRNA in adipose tissue and adipocytes were up-regulated in high cholesterol group compared with those of control group(P
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Objective To observe the effects of palmitic acid (PA) and fenofibrate (FF) on rat islets. Methods Rat islets were isolated with collagenase digestion and divided into 6 groups: control group, PA0.2 group (with 0.2 mmol/L PA), PA0.4 group(with0.4mmol/LPA),FF group (with 5?10 -6 mol/L fenofibrate), PA0.2+FF group and PA0.4 +FF group. After being cultured 24 hours with PA in the presence or absence FF, baseline insulin secretion (BIS) and glucose stimulated insulin secretion (GSIS) were examined. The mRNA levels of insulin(INS), pancreas-duodenum homeobox-1 (PDX-1), glucose transport protein 2 (GLUT-2) and PPAR? were determined by RT-PCR or real-time PCR. Results (1)In both PA0.2 and PA0.4 groups, BIS was increased and GSIS increase was impaired as compared with control group (P0.05). Expressions of INS, PDX-1 ,GLUT2 and PPAR? mRNA were enhanced in PA0.2 +FF group and PA0.4 +FF group as compared with the two groups without FF respectively (all P
