Aim: To investigate the protective effect and the possible mechanism of curcumin on anti-atherosclerosis. Methods: Morphological changes of atherosclerotic lesions taken from apoE knockout (apoE -/-) mice were determined by hematoxylineosin staining. Intracellular lipid droplets and lipid levels were assayed by oil red O staining and HPLC. The protein expression of caveolin-1 was quantified by Western blotting. Translocation and the expression of sterol response element-binding protein-1 (SREBP-1) were indirectly detected by an immunofluorescence analysis. Results: The administration of 20 mg·kg -1 ·d -1 curcumin to apoE -/-mice for 4 months induced a 50% reduction of atherosclerotic lesions and yielded a 5-fold increase in the caveolin-1 expression level as compared to the model group. Rat vascular smooth muscle cells (VSMC) pretreated with 50 mg·L -1 ox-lipid density lipoprotein(ox-LDL) for 48 h increased cellular lipid contents, and stimulated SREBP-1 translocation, but decreased the caveolin-1 expression level. Lipid-loaded cells exposed to curcumin at various concentrations (12.5, 25, and 50 µmol·L -1 ) for different durations (0,6,12, 24, and 48 h) significantly diminished the number and area of cellular lipid droplets, total cholesterol, cholesterol ester, and free cholesterol accompanying the elevation of the caveolin-1 expression level (approximately 3-fold); the translocation of SREBP-1 from the cytoplasm to the nucleus was inhibited compared with the models. Lipid-loaded VSMC exposed to N-acetylLeu-Leu-norleucinal, a SREBP-1 protease inhibitor, showed increased nuclear translocation of SREBP-1, reduced caveolin-1 expression level, and upregulated cellular lipid levels. Conclusion: Curcumin inhibits ox-LDL-induced cholesterol accumulation in cultured VSMC through increasing the caveolin-1 expression via the inhibition of nuclear translocation of SREBP-1.

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ObjectiveThis study aims to study the correlation between serum β2-glycoprotein I (β2-GPI)/oxidized low-density lipoprotein (oxLDL) and the risk of cerebral infarction in patients with type 2 diabetes (T2DM).MethodsFrom January 2019 to March 2021, 56 patients with T2DM combined with cerebral infarction were chosen as a diabetic cerebral infarction (DCI) group, and 60 patients with simple T2DM were chosen as a T2DM group. In addition, 60 healthy volunteers were recruited as a control group. The essential information of each group was collected, and the serum β2-GPI/oxLDL and inflammatory factor levels in each group were compared. The clinical factors that affect the risk of ischemic cerebral infarction in patients with T2DM were analyzed by a logistic model.ResultsCompared with the control group, the level of serum β2-GPI/oxLDL in the T2DM and DCI groups increased significantly, P < 0.001. Compared with the T2DM group, the serum β2-GPI/oxLDL level in the DCI group increased significantly, P < 0.05. The result of Pearson’s correlation analysis showed that serum β2-GPI/oxLDL was positively correlated with total cholesterol, triglycerides, fasting blood glucose, 2-h postprandial blood glucose, glycosylated hemoglobin, interleukin-6, and tumor necrosis factor (TNF)-α (all P’s < 0.05). Serum TNF-α and β2-GPI/oxLDL were independent risk variates for DCI (P < 0.05). Based on the receiver operating characteristic curve analysis, the values of the area under the curve for TNF-α, serum β2-GPI/oxLDL, and the combined diagnosis of DCI were 0.653 (0.552–0.753), 0.680 (0.583–0.777), 0.739 (0.647–0.831), respectively.ConclusionIn DCI patients, the levels of serum oxLDL/β2-GPI are significantly increased. Serum oxLDL/β2-GPI is an independent risk factor that affects the occurrence of DCI. In addition, the serum β2-GPI/oxLDL level implicates the lipid metabolism and inflammatory status of the internal environment of DCI patients to a certain extent.