Preparation and Application of pH-Sensitive Film Containing Anthocyanins Extracted from Lycium ruthenicum Murr.

A new pH-sensitive film was developed using Artemisia sphaerocephala Krasch. gum (ASKG), soybean protein isolate (SPI), and natural anthocyanin extracted from Lycium ruthenicum Murr. The film was prepared by adsorbing anthocyanins dissolved in an acidified alcohol solution on a solid matrix. ASKG and SPI were used as the solid matrix for the immobilization of the Lycium ruthenicum Murr. anthocyanin extract, which was absorbed into the film as a natural dye using the facile-dip method. Regarding the mechanical properties of the pH-sensitive film, the tensile strength (TS) values increased approximately 2-5-fold, but the elongation at break (EB) values decreased significantly by about 60% to 95%. With the increase in anthocyanin concentration, the oxygen permeability (OP) values first decreased by about 85%, and then increased by about 364%. The water vapor permeability (WVP) values increased by about 63%, and then decreased by about 20%. Colorimetric analysis of the films revealed variations in color at different pH values (pH 2.0-10.0). Fourier-transform infrared (FT-IR) spectra and XRD patterns indicated compatibility among ASKG, SPI, and anthocyanin extracts. In addition, an application test was conducted to establish a correlation between film color change and carp meat spoilage. At storage temperatures of 25 °C and 4 °C, when the meat was totally spoiled, the TVB-N values reached 99.80 ± 2.53 mg/100 g and 58.75 ± 1.49 mg/100 g, and the film's color changed from red to light brown and from red to yellowish green, respectively. Therefore, this pH-sensitive film could be used as an indicator to monitor the freshness of meat during storage.

Myeloid-restricted CD68 deficiency attenuates atherosclerosis via inhibition of ROS-MAPK-apoptosis axis.

In atherosclerosis, macrophages derived from blood monocytes contribute to non-resolving inflammation, which subsequently primes necrotic core formation, and ultimately triggers acute thrombotic vascular disease. Nevertheless, little is known about how inflammatory cells, especially the macrophages fuel atherosclerosis. CD68, a unique class D scavenger receptor (SRD) family member, is specifically expressed in monocytes/macrophages and remarkably up-regulated upon oxidized low-density lipoprotein (ox-LDL) stimulation. Nonetheless, whether and how myeloid-specific CD68 affects atherosclerosis remains to be defined. To determine the essential in vivo role and mechanism linking CD68 to atherosclerosis, we engineered global and myeloid-specific CD68-deficient mice on an ApoE-null background. On Western diet, both the mice with global and the myeloid-restricted deletion of CD68 on ApoE-null background attenuated atherosclerosis, accompanied by diminished immune/inflammatory cell burden and necrotic core content, but increased smooth muscle cell content in atherosclerotic plaques. In vitro experiments revealed that CD68 deficiency in macrophages resulted in attenuated ox-LDL-induced macrophage apoptosis. Additionally, CD68 deficiency suppressed ROS production, while removal of ROS can markedly reversed this effect. We further showed that CD68 deficiency affected apoptosis through inactivation of the mitogen-activated protein kinase (MAPK) pathway. Our findings establish CD68 as a macrophage lineage-specific regulator of "ROS-MAPK-apoptosis" axis, thus providing a previously unknown mechanism for the prominence of CD68 as a risk factor for coronary artery disease. Its therapeutic inhibition may provide a potent lever to alleviate the cardiovascular disease.

Slfn4 deficiency improves MAPK-mediated inflammation, oxidative stress, apoptosis and abates atherosclerosis progression in apolipoprotein E-deficient mice.

BACKGROUND AND AIMS: Atherosclerosis, a progressive inflammatory disease characterized by elevated inflammation and lipid accumulation in the aortic endothelium, arises in part from the infiltration of inflammatory cells into the vascular wall. However, it is not fully defined how inflammatory cells, especially macrophages, affect the pathogenesis of atherosclerosis. Schlafen4 (Slfn4) mRNA is remarkably upregulated upon ox-LDL stimulation in macrophages. Nonetheless, the role of Slfn4 in foam cell formation remains unclear. METHODS: To determine whether and how Slfn4 regulates lesion macrophage function during atherosclerosis，we engineered ApoE-/-Slfn4-/- double-deficient mice on an ApoE-/- background and evaluated the deficiency of Slfn4 expression in atherosclerotic lesion formation in vivo. RESULTS: Our results demonstrate that total absence of SLFN4 and the bone marrow-restricted deletion of Slfn4 in ApoE-/- mice remarkably diminish inflammatory cell numbers within arterial plaques as well as limit development of atherosclerosis in moderate hypercholesterolemia condition. This is linked to a marked reduction in the expression of proinflammatory cytokines, the generation of the reactive oxygen species (ROS) and the apoptosis of cells. Furthermore, the activation of MAPKs and apoptosis signaling pathways is compromised in the absence of Slfn4. CONCLUSIONS: These findings demonstrate a novel role of Slfn4 in modulating vascular inflammation and atherosclerosis, highlighting a new target for the related diseases.