Scutellarin inhibits oleic acid induced vascular smooth muscle foam cell formation via activating autophagy and inhibiting NLRP3 inflammasome activation.

Abnormalities in vascular smooth muscle cells (VSMCs) are pivotal in the pathogenesis of cardiovascular pathologies such as atherosclerosis and hypertension. Scutellarin (Scu), a flavonoid derived from marigold flowers, exhibits a spectrum of biological activities including anti-inflammatory, antioxidant, antitumor, immunomodulatory and antimicrobial effects. Notably, Scu has demonstrated the capacity to mitigate vascular endothelial damage and prevent atherosclerosis via its antioxidative properties. Nevertheless, the influence of Scu on the formation of VSMC-derived foam cells remains underexplored. In this study, Scu was evidenced to efficaciously attenuate oleic acid (OA)-induced lipid accumulation and the upregulation of adipose differentiation-associated protein Plin2 in a dose- and time-responsive manner. We elucidated that Scu effectively diminishes OA-provoked VSMC foam cell formation. Further, it was established that Scu pretreatment augments the protein expression of LC3B-II and the mRNA levels of Map1lc3b and Becn1, concurrently diminishing the protein levels of the NLRP3 inflammasome compared to the OA group. Activation of autophagy through rapamycin attenuated NLRP3 inflammasome protein expression, intracellular lipid droplet content and Plin2 mRNA levels. Scu also counteracted the OA-induced decrement of LC3B-II levels in the presence of bafilomycin-a1, facilitating the genesis of autophagosomes and autolysosomes. Complementarily, in vivo experiments revealed that Scu administration substantially reduced arterial wall thickness, vessel wall cross-sectional area, wall-to-lumen ratio and serum total cholesterol levels in comparison to the high-fat diet model group. Collectively, our findings suggest that Scu attenuates OA-induced VSMC foam cell formation through the induction of autophagy and the suppression of NLRP3 inflammasome activation.

Nomograms for predicting the overall and cancer-specific survival of patients with classical Hodgkin lymphoma: a SEER-based study.

The aim of this study was to establish nomograms, based on significant clinicopathologic parameters, for predicting the overall survival (OS) and the cancer-specific survival (CSS) of patients with classical Hodgkin lymphoma (CHL). The data of 43,330 CHL patients, diagnosed between 1983 and 2014, were obtainedfrom the database of the Surveillance, Epidemiology, and End Results (SEER) program. These patients were randomly divided into training (n = 30,339) and validation (n = 12,991) cohorts. The Kaplan-Meier method and Cox proportional hazards regression model were used to evaluate the prognostic effects of multiple clinicopathologic parameters on survival. Significant prognostic factors were combined to build nomograms. The predictive performance of nomograms was evaluated using the index of concordance (C-index) and calibration curves. In the training cohort, on univariate and multivariate analyses, age at diagnosis, gender, race, Ann Arbor stage, and histological type significantly correlated with the survival outcomes. These characteristics were used to establish nomograms. The nomograms showed good accuracy in predicting 1-, 5-, and 10-year OS and CSS, with a C-index of 0.794 (95% confidence interval [CI], 0.789-0.799) for OS and 0.760 (95% CI, 0.753-0.767) for CSS. In the validation cohort, the C-index for nomogram-based predictions was 0.787 (95% CI, 0.779-0.795) for OS and 0.769 (95% CI, 0.758-0.780) for CSS. All calibration curves revealed excellent consistency between predicted and actual survival. In summary, novel nomograms were established and validated to predict OS and CSS for patients with CHL. These new prognostic models could aid in improved prediction of survival outcomes leading to reasonable treatment recommendations.

[Establishment and analysis of chronic periodontitis and atherosclerosis model in Wistar rat].

OBJECTIVE: To investigate the possible correlation between atherosclerosis and chronic periodontitis by establishing an animal model of chronic periodontitis and atherosclerosis in Wistar rat. METHODS: Sixty male Wistar rats were divided into four groups: A (control group), B (chronic periodontitis group), C (atherosclerosis group), D (chronic periodontitis accompany with atherosclerosis group). Every group was accepted the corresponding treatment. Animals were sacrificed after 12 weeks. The periodontal index, levels of serum total cholesterol (TC) and low-density lipoprotein (LDL), the concentration of TNF-alpha and matrix metalloproteinase (MMP-3) were examined. The severity of chronic periodontitis and atherosclerosis was quantified by histopathology. The date were statistically analyzed. RESULTS: Through detection of periodontal tissue of experimental teeth, serum and histopathology, animal models were successful. Histopathologic observation revealed:obvious inflammation of periodontal tissue was observed in group B and D. Attachment loss level in group B [(137.86 +/- 28.39) microm] and D [(162.36 +/- 22.69) microm] was higher than that in group A [(4.26 +/- 1.07) microm] and C [(68.07 +/- 18.25) microm] (P < 0.05), and that in group C was higher than group A (P < 0.05). Atherosclerotic lesions of abdominal aorta were formed in group C and D. The level of TC, LDL in group C and D was higher than that in group A and B (P < 0.05), and that in group D was higher than group C (P < 0.05). Animals in group B and D showed higher level of TNF-alpha, MMP-3 in serum than that in group A and C (P < 0.05). There was no correlation between the level of MMP-3 and TC (P = 0.971) or LDL (P = 0.604). CONCLUSIONS: Chronic periodontitis may be a risk factor and contribute to the pathogenesis of atherosclerosis. MMP-3 may be an independent risk factor of atherosclerosis exclude TC and LDL.