Abstract:Abnormalities in lipid metabolism induce myocardial structural and functional disorders, leading to the development of diabetic cardiomyopathy (DCM), which has become a hotspot in current DCM research. The transmembrane glycoprotein CD36 is a multifunctional membrane protein that facilitates fatty acid transport, which is involved in the regulation of cardiac lipid metabolism. CD36 signaling plays a key role in the pathogenesis of DCM mediated cardiac injuries. This article summarizes the structure of CD36 and its role in specific cell types, and further explores the pathophysiological role of CD36 in DCM, proposing that targeting CD36 may prove to be a potential pharmacological strategy in the prevention and treatment of DCM.

Abstract:Aim To investigate the binding mechanism of fatty acid translocase FAT/CD36 and long chain fatty acid. Methods ELISA was used to analyze the intensity mechanism of the purity of FAT/CD36 binding with different fatty acid, molecular simulation docking was used to further verify the binding mechanism and analyze its possible binding sites. Results ELISA proved that the recombinant protein FAT/CD36 with different types of long chain fatty acids showed specific binding, binding values for oleic acid＞palmitic acid＞palmitoleic acid＞myristic acid＞stearic acid. Molecular simulation docking further confirmed that FAT/CD36 receptor protein mainly combines with oleic acid, palmitic acid and palmitoleic acid. And the binding site was located in the extracellular structure of the FAT/CD36 receptor protein Arg183-Lys-Gly-Lys-Arg-Asn-Leu-Ser-Tyr238 region consisting of the active pocket. Conclusion FAT/CD36, as the main receptor of long chain fatty acid transport, may transport oleic acid, palmitic acid and palmitoleic acid.

Abstract:CD36 is a multifunctional transmembrane glycoprotein that binds to oxidized low density lipoprotein to induce monocyte transformation into foam cells and promotes the formation of atherosclerosis through inflammatory response, oxidative stress, platelet activation, macrophage trapping. Inhibition of CD36 expression or interference with its associated signaling pathways can significantly alleviate the severity of atherosclerosis. In addition, the high expression of CD36 in the tongue, nasal cavity, small intestine and brain promotes the bodys intake and absorption of lipids, and increases the risk factors of metabolic diseases. Serum soluble CD36 is found as a component of circulating microparticles and may be as a predictor for atherosclerotic disease.

Abstract:Aim To study the effect of renal artery radiofrequency ablation in endarterium or adventitia on renal artery atherosclerosis by detecting expression levels of renal artery macrophage scavenger receptor (CD36 and SR-A). Methods 14 healthy beagles (7 male, 7 female) were randomly divided into experimental group (n=10) and control group (n=4), and two arteries in every beagle of the experimental group were randomly assigned to endarterium group(10 artery) and adventitial group(10 artery). At 1 month and 3 months follow-up, renal artery angiography was performed to observe the renal artery morphological change; HE staining and immunohistochemical staining were used to observe the renal artery pathological change; Western blot was used to detect the expression levels of renal artery macrophage scavenger receptor (CD36 and SR-A). Results (1) At 1 month follow-up, 1 case of obvious renal artery stenosis was found in endarterium group. (2) In the experimental group after renal denervation, intimal structure of renal artery was discontinued by HE staining, but no change was found in the control group; Immunohistochemistry showed the higher expression of CD36 in renal artery of experimental group. (3) The expression of scavenger receptors (CD36 and SR-A) in renal artery:①At 1 month follow-up, the expression levels of scavenger receptor CD36 and SR-A were significantly higher in endarterium group (n=5) and adventitia group (n=5) than that in the control group (n=4) (P<0.001); And the expression levels of scavenger receptor CD36 and SR-A were significantly higher in endarterium group (n=5) than that in adventitia group (P=0.040 and P=0.007); ②At 3 months follow-up, the expression levels of scavenger receptor CD36 and SR-A were significantly higher in endarterium group (n=5) and adventitia group (n=5) than that in control group (n=4) (P<0.001); And the expression levels of scavenger receptor CD36 and SR-A were significantly higher in endarterium group (n=5) than that in adventitia group (n=5) (P<0.001). Conclusion Renal artery stenosis may appear after renal denervation, and it was easier to lead to renal artery stenosis after renal denervation in endarterium;The structure of renal artery endarterium may be damaged (thickening and discontinuous) after renal denervation; and it is higher in endarterium, so it has the potential risk of renal atherosclerosis after renal denervation.

Abstract:The formation and inhibited emigration of foam cells are the key events in malignant remodeling of artery plaques. Advanced glycation end products (AGE) play an important role in the course of diabetes-accelerating atherosclerotic progression. Based on the latest international research progress and our existing results, this paper elaborated the mechanism of CD36 modulating foam cell emigration from plaques inhibited by Nε-carboxymethyl-Lysine, which would provide a new starting point for the treatment strategy of targeting foam cell migration mechanism in the future.

Abstract:Aim To evaluate the effect of Alisol A 24-acetate on the protein expression of lipid metabolism factors ATP-binding cassette transporter A1 (ABCA1), class B scavenger receptor (CD36) and inflammatory factors extracellular matrix metalloproteinase inducer (CD147), matrix metalloproteinase-9 (MMP-9) in oxidized low density liprotein (ox-LDL)-stimulated rat peritoneal macrophages. Methods Rat peritoneal macrophages were respectively treated with 50 mg/L ox-LDL and 10 mg/L Dil-ox-LDL, and intervened with 10 mg/L Alisol A 24-acetate. Dil-ox-LDL accumulation in macrophages was observed with fluorescence microscope. The protein expression of ABCA1, CD147, CD36 and MMP-9 were detected by Western blot. Results After induced with 10 mg/L Dil-ox-LDL, a large number of Dil-ox-LDL accumulation was observed in peritoneal macrophages of rats. Intracellular Dil-ox-LDL accumulation was significantly reduced after 10 mg/L Alisol A 24-acetate intervention. Compared with the control group, the protein expressions of ABCA1, CD36 and CD147, MMP-9 were significantly increased in peritoneal macrophages after induced with 50 ox-LDL mg/L. After 10 mg/L Alisol A 24-acetate intervention, the protein expression of ABCA1 was increased further (P<0.01), and protein expressions of CD36, CD147 and MMP-9 were significantly inhibited (P<0.05 or P<0.01). Conclusions Alisol A 24-acetate can increase the expression of lipid metabolic factor ABCA1, inhibit the expression of CD36, and reduce cholesterol accumulation in macrophages. Also it can inhibit the secretion of inflammatory factors CD147 and MMP-9.

Abstract:Aim To explore the effects of nuciferine on the expressions of CD36 and peroxisome proliferator-activated receptor γ （PPARγ） in THP-1 derived macrophages,and the signal transduction pathway. Methods THP-1 derived macrophages were randomly divided into groups of normal,oxidized low density lipoprotein （ox-LDL）,nuciferine and ciglitazone. Macrophage cells were valued by oil red O staining. The expressions of CD36 and PPARγ were measured by RT-PCR and Western blot,respectively. Results Compared with normal group,lipid droplets were increased while mRNA and protein expressions of CD36 and PPARγ were upregulated in ox-LDL group. Compared with ox-LDL group,lipid droplets were decreased while mRNA and protein expressions of CD36 and PPARγ were downregulated in nuciferine group. Compared with nuciferine group,lipid droplets had no difference while mRNA and protein expressions of CD36 and PPARγ were upregulated in ciglitazone group. Conclusions Nuciferine downregulates CD36 expression in THP-1 derived macrophages,lessen the degree of foam formation. Nuciferine downregulates CD36 expression by downregulating PPARγ expression.

Abstract:Aim To investigate the effect of high glucose on regulating the expression of CD36 and lipid accumulation in THP-1 macrophages. Methods THP-1 macrophages were incubated with different concentrations of D-glucose （5.6, 11, 20, 30 and 35 mmol/L）, 50 mg/L oxidized low density lipoprotein （ox-LDL）, 50 mg/L ox-LDL＋20 mmol/L D-glucose for 24 h. Total cholesterol content in THP-1 macrophages was determined by high performance liquid chromatography, the lipid accumulation was detected by oil red O stain. CD36 mRNA and protein levels were determined by reverse transcription-polymerase chain reaction （RT-PCR） and Western blot, respectively. Results With the increase of D-glucose concentration treating THP-1 macrophages, the expression of CD36 mRNA and protein were up-regulated gradually （P<0.05）, high glucose in concert with ox-LDL induced the expression of CD36 mRNA and protein in THP-1 macrophages （P<0.05）, and enhanced the level of total cholesterol （P<0.05）. Conclusion High glucose can up-regulate the expression of CD36 and increase the lipid accumulation in THP-1 macrophages.

Abstract:Aim To investigate the effect of high glucose on the expression of CD36 and peroxisome proliferator-activated receptor gamma （PPARγ） regulated by high density lipoprotein （HDL） in THP-1 macrophage. Methods THP-1 macrophages were incubated with 50 mg/L ox-LDL, 50 mg/L ox-LDL+50 mg/L HDL, 50 mg/L ox-LDL+50 mg/L HDL+20 mmol/L D-Glucose, 50 mg/L HDL, 50 mg/L HDL+20 mmol/L D-Glucose for 24 h. The lipid accumulation was detected by oil red O stain. CD36 and PPARγ mRNA were determined by reverse transcription-polymerase chain reaction （RT-PCR）, respectively. CD36, PPARγ and p-PPARγ protein was determined by Western Blot. Results

Abstract:Aim To investigate the effect of peroxisome proliferator activated receptor γ （PPARγ） on the expression of CD36 and the lipid accumulation induced by high glucose in THP-1 macrophages. Methods THP-1 macrophages were incubated with 20 mmol/L D-glucose, 10 mmol/L GW9662, and 50 mg/L oxidized low density lipoprotein （ox-LDL） for 24 h, combinated or respectively. The total cholesterol contents in THP-1 macrophages were determined by high performance liquid chromatography, and the lipid accumulation was detected by oil red O stain. CD36 and PPARγ mRNA level were determined by reverse transcription polymerase chain reaction （RT-PCR）, respectively. CD36 and PPARγ protein level were determined by Western blot. Results GW9662 significantly inhibited the expression of CD36 and lipid accumulation induced by high glucose in THP-1 macrophages. The expression of CD36 mRNA and protein was significantly suppressed by GW9662 （P<0.05）, intracellular lipid decreased obviously and the total cholesterol in THP-1 macrophages was markedly reduced subsequently （P<0.05）. Conclusion High glucose induces CD36 expression and lipid accumulation through the modulation of PPARγ in THP-1 macrophages.