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Vascular calcification (VC) is an accurate risk factor and predictor of adverse cardiovascular events; however, there is currently no effective therapy to specifically prevent VC progression. Capsaicin (Cap) is a bioactive alkaloid isolated from Capsicum annuum L., a traditional medicinal and edible plant that is beneficial for preventing cardiovascular diseases. However, the effect of Cap on VC remains unclear. This study aimed to explore the effects and related mechanisms of Cap on aortic calcification in a mouse and on Pi-induced calcification in vascular smooth muscle cells (VSMCs). First, we established a calcification mouse model with vitamin D3 and evaluated the effects of Cap on calcification mice using von Kossa staining, calcium content, and alkaline phosphatase activity tests. The results showed that Cap significantly improved calcification in mice. VSMCs were then cultured in 2.6 mM Na2HPO4 and 50 μg/mL ascorbic acid for 7 days to obtain a calcification model, and we investigated the effects and mechanisms of Cap on VSMCs calcification by assessing the changes of calcium deposition, calcium content, and subsequent VC biomarkers. These results showed that Cap alleviated VSMCs calcification by upregulating the expressions of TRPV1. Moreover, Cap reduced the expression of Wnt3a and β-catenin, whereas DKK1 antagonised the inhibitory effect of Cap on VSMC calcification. This study is the first to offer direct evidence that Cap inhibits the Wnt/β-catenin signaling pathway by upregulating the expression of the TRPV1 receptor, resulting in the decreased expression of Runx2 and BMP-2, thereby reducing VSMC calcification. Our study may provide novel strategies for preventing the progression of VC. This could serve as a theoretical basis for clinically treating VC with spicy foods.

Abstract Introduction This prospective observational study with a control group aimed to compare the plasma levels of long non-coding RNA (lncRNA) LIPCAR between patients with acute cerebral infarction (ACI) and healthy controls, and to assess the prognostic abilities of LIPCAR for adverse outcomes of patients with ACI at 1-year follow-up. Methods Eighty patients with ACI, of whom 40 had large artery atherosclerosis (LAA) and 40 had cardioembolism (CE) and who were hospitalized at Xi'an No. 1 Hospital from July 2019 to June 2020, were selected as the case group. Age- and sex-matched non-stroke patients from the same hospital throughout the same time period were chosen as the control group. Real-time quantitative reverse transcription polymerase chain reaction was used to measure the levels of plasma lncRNA LIPCAR. The correlations of LIPCAR expression among the LAA, CE, and control groups were assessed using Spearman’s correlation analysis. Curve fitting and multivariate logistic regression were used to analyze the LIPCAR levels and 1-year adverse outcomes of patients with ACI and its subtypes. Results The expression of plasma LIPCAR in the case group was noticeably higher than that of the control group (2.42 ± 1.49 vs. 1.00 ± 0.47, p

We studied the sensitivity of several human cancer cell strains (HeLa, HT1080, SPC-A1, and ACHN) and normal cell strains (MRC-5 and Wish) to mumps virus (MuV) S79, a live attenuated vaccine strain. These cells exhibited a differential sensitivity to infection with MuV, and the susceptible sequences were ACHN > HeLa > HT1080 > SPC-A1 > Wish > MRC-5. In experiments in vivo, nude mice with HT1080 fibrosarcoma xenografts were randomly divided into three groups for intratumoral treatment with MuVS79, UV-inactivated MuVS79, and PBS. At 107 PFU, live MuVS79 injection caused in 7 of 9 mice complete regression by day 15 while rapid tumor growth occurred in all 9 mice treated with PBS. Rapid tumor progression also occurred in all 8 mice treated with UV-inactivated virus; however, tumor growth was delayed in the logarithmic phase relative to the PBS-treated tumors. Copyright © 2005 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

We studied the sensitivity of several human cancer cell strains (HeLa, HT1080, SPC-A1, and ACHN) and normal cell strains (MRC-5 and Wish) to mumps virus (MuV) S79, a live attenuated vaccine strain. These cells exhibited a differential sensitivity to infection with MuV, and the susceptible sequences were ACHN > HeLa > HT1080 > SPC-A1 > Wish > MRC-5. In experiments in vivo, nude mice with HT1080 fibrosarcoma xenografts were randomly divided into three groups for intratumoral treatment with MuVS79, UV-inactivated MuVS79, and PBS. At 107 PFU, live MuVS79 injection caused in 7 of 9 mice complete regression by day 15 while rapid tumor growth occurred in all 9 mice treated with PBS. Rapid tumor progression also occurred in all 8 mice treated with UV-inactivated virus; however, tumor growth was delayed in the logarithmic phase relative to the PBS-treated tumors. Copyright © 2005 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]