Search

Summary: Solid‐state fermentation (SSF) is an economically viable processing technique to improve the bioactive content from agricultural by‐products. The impacts of SSF by Aspergillus niger (AN) and Lactobacillus plantarum (LP) on the physicochemical and functional properties of wheat bran and whole wheat bread were investigated in this study. Compared with unfermented wheat bran, the pH of fermented wheat bran decreased significantly, and the titrated acidity increased significantly. The water absorption index, water solubility index and swelling capacity of wheat bran were significantly increased after fermentation. Besides, the free‐radical scavenging activities for DPPH, ABTS and the total antioxidant capacity of wheat bran were notably increased after SSF. Moreover, the content of alkylresorcinols (ARs), total phenolics and flavonoids compounds in wheat bran were enhanced by 137.85%, 52.87% and 95.6%, respectively, after fermentation. The content of aflatoxin B1, deoxynivalenol, zearalenone and ochratoxin A were decreased by 76.34%, 18.67%, 34.48% and 20.46%, respectively. SSF enhanced the content of ARs, total phenols and flavonoids in the reconstituted whole wheat bread by 136.55%, 54.55% and 97.74%, respectively. Whereas, the hardness and chewiness of the bran‐rich bread were decreased by 75.2% and 92.41%, respectively. Additionally, the sensory evaluation score, specific volume and the overall score of reconstituted bread were significantly improved. Taken together, SSF by AN and LP could improve the processing value of wheat bran and might be a feasible solution to upgrade whole wheat product quality. [ABSTRACT FROM AUTHOR]

Multiple phenolic substances have been shown to promote SIRT3 expression, however, few studies have focused on the effects of these phenolics on SIRT3 enzyme activity. This study constructed a variety of reaction systems to elucidate the mechanisms by which different polyphenols affect SIRT3 enzyme activity. The results showed that acP53 317 – 320 was the most suitable substrate among the five acetylated peptide substrates (K cat / K m = 74.85 ± 1.86 M−1•s−1). All the phenolic compounds involved in the experiment inhibited the enzymatic activity of SIRT3, and the lowest IC 50 among them was quercetin (0.12 ± 0.01 mM) and the highest was piceatannol (1.29 ± 0.08 mM). Their inhibition types were mainly competitive and mixed. In addition, piceatannol was found to be a natural SIRT3 agonist by enzyme kinetic analysis and validation of deacetylation efficiency. This study will provide a useful reference for polyphenol modulation of SIRT3 dosage, as well as the development and application of polyphenol-based SIRT3 activators and agonists. • The IC 50 for inhibition of SIRT3 enzyme activity by different polyphenols was detected. • Interaction mechanisms between different polyphenols and SIRT3 were analyzed. • Mechanistic analysis of piceatannol enhancing the enzymatic activity of SIRT3. • A strategy for agonist or inhibitor screening of SIRT3 was constructed. [ABSTRACT FROM AUTHOR]

Multiple phenolic substances have been shown to promote SIRT3 expression, however, few studies have focused on the effects of these phenolics on SIRT3 enzyme activity. This study constructed a variety of reaction systems to elucidate the mechanisms by which different polyphenols affect SIRT3 enzyme activity. The results showed that acP53 317 – 320 was the most suitable substrate among the five acetylated peptide substrates (K cat / K m = 74.85 ± 1.86 M−1•s−1). All the phenolic compounds involved in the experiment inhibited the enzymatic activity of SIRT3, and the lowest IC 50 among them was quercetin (0.12 ± 0.01 mM) and the highest was piceatannol (1.29 ± 0.08 mM). Their inhibition types were mainly competitive and mixed. In addition, piceatannol was found to be a natural SIRT3 agonist by enzyme kinetic analysis and validation of deacetylation efficiency. This study will provide a useful reference for polyphenol modulation of SIRT3 dosage, as well as the development and application of polyphenol-based SIRT3 activators and agonists. • The IC 50 for inhibition of SIRT3 enzyme activity by different polyphenols was detected. • Interaction mechanisms between different polyphenols and SIRT3 were analyzed. • Mechanistic analysis of piceatannol enhancing the enzymatic activity of SIRT3. • A strategy for agonist or inhibitor screening of SIRT3 was constructed. [ABSTRACT FROM AUTHOR]

Obesity and its related complications pose an increasing threat to human health; however, targetable obesity‐related membrane receptors are not yet elucidated. Here, the membrane receptor CD146 is demonstrated to play an essential role in obesity. In particular, CD146 acts as a new adipose receptor for angiopoietin‐like protein 2 (ANGPTL2), which is thought to act on endothelial cells to activate adipose inflammation. ANGPTL2 binds to CD146 to activate cAMP response element‐binding protein (CREB), which then upregulates CD146 during adipogenesis and adipose inflammation. CD146 is present in preadipocytes and mature adipocytes, where it is mediated by its ligands ANGPTL2 and galectin‐1. In preadipocytes, CD146 ablation suppresses adipogenesis, whereas the loss of CD146 in mature adipocytes suppresses lipid accumulation and enhances energy expenditure. Moreover, anti‐CD146 antibodies inhibit obesity by disrupting the interactions between CD146 and its ligands. Together, these findings demonstrate that ANGPTL2 directly affects adipocytes via CD146 to promote obesity, suggesting that CD146 can be a potential target for treating obesity. [ABSTRACT FROM AUTHOR]

Obesity and its related complications pose an increasing threat to human health; however, targetable obesity‐related membrane receptors are not yet elucidated. Here, the membrane receptor CD146 is demonstrated to play an essential role in obesity. In particular, CD146 acts as a new adipose receptor for angiopoietin‐like protein 2 (ANGPTL2), which is thought to act on endothelial cells to activate adipose inflammation. ANGPTL2 binds to CD146 to activate cAMP response element‐binding protein (CREB), which then upregulates CD146 during adipogenesis and adipose inflammation. CD146 is present in preadipocytes and mature adipocytes, where it is mediated by its ligands ANGPTL2 and galectin‐1. In preadipocytes, CD146 ablation suppresses adipogenesis, whereas the loss of CD146 in mature adipocytes suppresses lipid accumulation and enhances energy expenditure. Moreover, anti‐CD146 antibodies inhibit obesity by disrupting the interactions between CD146 and its ligands. Together, these findings demonstrate that ANGPTL2 directly affects adipocytes via CD146 to promote obesity, suggesting that CD146 can be a potential target for treating obesity. [ABSTRACT FROM AUTHOR]

CAR-like membrane protein (CLMP) is a tight junction-associated protein whose mutation is associated with congenital short bowel syndrome (CSBS), but its functions in colorectal cancer (CRC) remain unknown. Here, we demonstrate that CLMP is rarely mutated but significantly decreased in CRC patients, and its deficiency accelerates CRC tumorigenesis, growth, and resistance to all- trans retinoic acid (ATRA). Mechanistically, CLMP recruits β-catenin to cell membrane, independent of cadherin proteins. CLMP-mediated β-catenin translocation inactivates Wnt(Wingless and INT-1)/β-catenin signaling, thereby suppressing CRC tumorigenesis and growth in Apc Min/+ , azoxymethane/dextran sodium sulfate (AOM/DSS), and orthotopic CRC mouse models. As a direct target of Wnt/β-catenin, cytochrome P450 hydroxylase A1 (CYP26A1)—an enzyme that degrades ATRA to a less bioactive retinoid—is upregulated by CLMP deficiency, resulting in ATRA-resistant CRC that can be reversed by administering CYP26A1 inhibitor. Collectively, our data identify the anti-CRC role of CLMP and suggest that CYP26A1 inhibitor enable to boost ATRA's therapeutic efficiency. [Display omitted] • CLMP is downregulated in CRC, and CLMP deficiency enhances colorectal carcinogenesis • CLMP inhibits Wnt/β-catenin signaling by recruiting β-catenin to the cell membrane • CLMP suppresses CYP26A1-mediated ATRA degradation • CYP26A1 inhibitor enhances the suppressive effect of ATRA on CRC treatment Wu and Zhang et al. identify that CAR-like membrane protein (CLMP) functions as a tumor suppressor in CRC. Mechanistically, CLMP recruits β-catenin to the cell membrane, thereby suppressing Wnt/β-catenin signaling and reducing the expression of CYP26A1, which degrades ATRA into less bioactive retinoid, consequently enhancing the response of CRC to ATRA treatment. [ABSTRACT FROM AUTHOR]

COVID-19, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), emerged as a global health threat in 2019. An important feature of the disease is that multiorgan symptoms of SARS-CoV-2 infection persist after recovery. Evidence indicates that people who recovered from COVID-19, even those under the age of 65 years without cardiovascular risk factors such as smoking, obesity, hypertension, and diabetes, had a significantly increased risk of cardiovascular disease for up to one year after diagnosis. Therefore, it is important to closely monitor individuals who have recovered from COVID-19 for potential cardiovascular damage that may manifest at a later stage. Ferroptosis is an iron-dependent form of non-apoptotic cell death characterized by the production of reactive oxygen species (ROS) and increased lipid peroxide levels. Several studies have demonstrated that ferroptosis plays an important role in cancer, ischemia/reperfusion injury (I/RI), and other cardiovascular diseases. Altered iron metabolism, upregulation of reactive oxygen species, and glutathione peroxidase 4 inactivation are striking features of COVID-19-related cardiovascular injury. SARS-CoV-2 can cause cardiovascular ferroptosis, leading to cardiovascular damage. Understanding the mechanism of ferroptosis in COVID-19-related cardiovascular injuries will contribute to the development of treatment regimens for preventing or reducing COVID-19-related cardiovascular complications. In this article, we go over the pathophysiological underpinnings of SARS-CoV-2-induced acute and chronic cardiovascular injury, the function of ferroptosis, and prospective treatment approaches. [Display omitted] • SARS-CoV-2 infection can cause severe cardiovascular injury through various mechanisms. • Ferroptosis may play a significant role in the pathogenesis of COVID-19-related cardiovascular injury. • The inhibition of ferroptosis may become a therapeutic target for COVID-19-related cardiovascular injury. [ABSTRACT FROM AUTHOR]