Background: NLR family pyrin domain containing 3 (NLRP3) inflammasome has been implicated in the development of atherosclerosis and several studies have suggested that inhibiting NLRP3 inflammasome could be a potential therapeutic approach to treat atherosclerosis. Baicalin is a flavone glycoside with anti-inflammation, anti-oxidative activities. The inhibition of NLRP3 inflammasome activation by baicalin has also been described. Therefore, the effects of baicalin on NLRP3 inflammasome activation and atherosclerosis were evaluated in present study. Methods: We established the apolipoprotein E-deficient atherosclerosis mice model. After baicalin treatment, the IL-1, IL-18, and reactive oxygen species (ROS) production, and the plaque area was monitored. We also measured the NLRP3, ASC, caspase-1, ICAM-1, and VCAM-1 expression in atherosclerosis mice after baicalin treatment. We silenced NLRP3 by administration of lentivirus expressing NLRP3 shRNA to atherosclerosis mice and monitored the IL-1, IL-18, and ROS production, and NLRP3 inflammasome activation. Results: Baicalin remarkably inhibited the production of IL-1, IL-18, mitochondria ROS, total ROS, ICAM-1, and VCAM-1. Baicalin reduced the expression of NLRP3 inflammasome and suppressed its activation. Baicalin significantly reduced the plaque area. Silencing NLRP3 resulted in decreased production of IL-1, IL-18, mitochondria ROS, total ROS, ICAM-1, and VCAM-1, and inhibition of NLRP3 inflammasome activation. Conclusion: Baicalin ameliorated atherosclerosis by inhibiting NLRP3 inflammasome.

Aim: The purposes of our study were to compare the clinical outcomes of human epidermal growth factor receptor 2 (HER2)-positive metastatic breast cancer (mBC) patients with or without trastuzumab treatment and HER2-negative patients, and to explore factors that might predict the survival benefit associated with trastuzumab treatment in HER2-positive breast cancer. Patients and Methods: A total of 421 patients with mBC were analyzed in this retrospective study. All patients had first-line chemotherapy with or without trastuzumab. They were classified into 3 groups according to their HER2 status and trastuzumab treatment: HER2-positive mBC patients with or without trastuzumab treatment and HER2-negative patents. Results: Trastuzumab administration in HER2-positive mBC patients significantly prolonged overall survival (33 vs. 26 months; P = 0.003) and led to a 49.8% reduction in death risk. In the subgroup analysis, HER2-positive patients with hormone receptor (HR)-negative status (29 vs. 17 months; P = 0.000) or visceral metastasis (30 vs. 21 months; P = 0.000) had more survival benefit when treated with trastuzumab. Conclusions: Trastuzumab administration significantly improved the overall survival in HER2-positive mBC patients, who gained a prognosis comparable to that of patients with HER2-negative disease. HR status and metastasis site might be important surrogate makers that predict survival benefit from trastuzumab-based treatment.

The expression level of UBQLN1 and prognosis in breast cancer is clarified for the first time and UBQLN1 seems to be a novel molecular marker to predict poor prognosis in breast cancer.