Oridonin, a well-known traditional Chinese herbal medicinal product isolated from Isodon rubescens (Hemsl.) H.Hara, has many potential properties, including anti-inflammatory and antioxidant activities. However, there is no evidence whether oridonin have a protective effect on atherosclerosis. This study focused on the effects of oridonin on oxidative stress and inflammation generated from atherosclerosis. The therapeutic effect on atherosclerosis was evaluated by intraperitoneal injection of oridonin in a high-fat fed ApoE−/− mouse model. We isolated mouse peritoneal macrophages and detected the effect of oridonin on oxidized low-density lipoprotein-induced lipid deposition. Oil red O staining, Masson's staining, dihydroethidium fluorescence staining, immunohistochemical staining, western blotting analysis, immunofluorescence, enzyme-linked immunosorbent assay and quantitative real-time PCR were used to evaluate the effect on atherosclerosis and explore the mechanisms. Oridonin treatment significantly alleviated the progression of atherosclerosis, reduced macrophage infiltration and stabilized plaques. Oridonin could significantly inhibit inflammation associated with NLRP3 activation. Oridonin significantly reduced oxidative stress by blocking Nrf2 ubiquitination and degradation. We also found that oridonin could prevent the formation of foam cells by increasing lipid efflux protein and reducing lipid uptake protein in macrophages. Oridonin has a protective effect on atherosclerosis in ApoE−/− mice, which may be related to the inhibition of NLRP3 and the stabilization of Nrf2. Therefore, oridonin may be a potential therapeutic agent for atherosclerosis.
Oridonin, a well-known traditional Chinese herbal medicinal product isolated from Isodon rubescens (Hemsl.) H.Hara, has many potential properties, including anti-inflammatory and antioxidant activities. However, there is no evidence whether oridonin have a protective effect on atherosclerosis. This study focused on the effects of oridonin on oxidative stress and inflammation generated from atherosclerosis. The therapeutic effect on atherosclerosis was evaluated by intraperitoneal injection of oridonin in a high-fat fed ApoE−/− mouse model. We isolated mouse peritoneal macrophages and detected the effect of oridonin on oxidized low-density lipoprotein-induced lipid deposition. Oil red O staining, Masson's staining, Dihydroethidium (DHE) fluorescence staining, Immunohistochemical staining, western blotting analysis, immunofluorescence, enzyme-linked immunosorbent assay (ELISA) and quantitative real-time PCR were used to evaluate the effect on atherosclerosis and explore the mechanisms. Oridonin treatment significantly alleviated the progression of atherosclerosis, reduced macrophage infiltration and stabilized plaques. Oridonin could significantly inhibit inflammation associated with NLRP3 activation. Oridonin significantly reduced oxidative stress by blocking Nrf2 ubiquitination and degradation. We also found that oridonin could prevent the formation of foam cells by increasing lipid efflux protein and reducing lipid uptake protein in macrophages. Oridonin has a protective effect on atherosclerosis in ApoE−/− mice, which may be related to the inhibition of NLRP3 and the stabilization of Nrf2. Therefore, oridonin may be a potential therapeutic agent for atherosclerosis.
Background: Carotid plaque is often an important factor in ischemic stroke after it changes from stable to vulnerable, and low-density lipoprotein cholesterol (LDL-c) and high-density lipoprotein cholesterol (HDL-c) are associated with plaque vulnerability. We aimed to investigate whether the LDL-c/HDL-c ratio, an easily available and novel biomarker, is associated with vulnerable plaques and enhances the warning effect on vulnerability compared to LDL-c or HDL-c alone. Methods: We conducted a retrospective study of 187 patients with severe CAS admitted to the Department of Vascular Surgery at Nanjing Drum Tower Hospital from January 2019 to July 2021. They were divided into a stable plaque group and a vulnerable plaque group according to carotid ultrasonography, carotid angiography (CTA), and plaque pathology. Baseline information was collected and compared between the two groups. Correlation analysis was used to determine the degree of correlation between clinical variables. Univariate and multifactor logistic regression analyses were used to examine independent risk factors for vulnerable plaque in patients with severe CAS. Receiver operating characteristic (ROC) curves were used to assess the capacity of LDL-c/HDL-c to predict the occurrence of vulnerable plaque. Results: The age of the vulnerable plaque group was 68.12 ± 8.90 years, with 85 males (89.91%); the age of the stable plaque group was 68.77 ± 8.43 years, with 70 males (89.74%). Multivariate logistic regression analysis showed that LDL-c/HDL-c, smoking and diabetes were independent risk factors for vulnerable plaque (all P <0.05). The risk of vulnerable plaque was 4.78-fold greater in the highest LDL-c/HDL-c quartile (≥ 2.63) than in the lowest quartile (≤ 1.31) (P-trend <0.001), and the area under the ROC curve for LDL-c/HDL-c (AUC=0.681, P <0.001) was higher than that for LDL-c and HDL-c. Conclusions: LDL-c/HDL-c, smoking and diabetes were independent risk factors for vulnerable plaque in patients with severe CAS, and LDL-c/HDL-c had a higher predictive value for the presence of vulnerable plaque compared with other lipid parameters.
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