Publications

Konjac glucomannan (KGM) has attracted extensive attention because of its biodegradable, non-toxic, harmless, and biocompatible features. Its gelation performance is one of its most significant characteristics and enables wide applications of KGM gels in food, chemical, pharmaceutical, materials, and other fields. Herein, different preparation methods of KGM gels and their microstructures were reviewed. In addition, KGM applications have been theoretically modeled for future uses.

Abstract Foam cells derived from macrophages and smooth muscle cells (SMCs) play a pivotal role in the progression of atherosclerosis. While phytosterols (PS) have demonstrated cholesterol‐lowering and anti‐inflammatory properties, their impact on foam cells remains elusive. Here, we investigated the effects of PS on foam cell formation, inflammatory responses, and lipid metabolism using both single‐cell RNA sequencing (scRNA‐seq) and functional assays. scRNA‐seq of aortic tissue from ApoE −/− mice revealed that PS supplementation reduced proinflammatory macrophages and SMC‐derived intermediate cells. Among the PS components, stigmasterol most effectively attenuated foam cell formation by suppressing oxidized low‐density lipoprotein (ox‐LDL) uptake and enhancing cholesterol efflux. Mechanistically, stigmasterol inhibited the inflammatory CD86 + macrophage polarization by activating the Adenosine Monophosphate‐Activated Protein Kinase (AMPK) pathway and inhibiting the NF‐κB/NLRP3 signaling axis. In SMCs, stigmasterol upregulated ABCA1 and ABCG1 expression, reduced lipid accumulation, and suppressed CD68 expression, thereby limiting trans‐differentiation into macrophage‐like foam cells. In vivo, stigmasterol reduced plaque burden, promoted anti‐inflammatory macrophage polarization, and inhibited SMC‐to‐macrophage transition in ApoE −/− mice. Collectively, these findings uncover a previously underexplored role of stigmasterol in modulating foam cell diversity and inflammation, providing mechanistic insight into the vascular protective effects of dietary PS.

ROS, RNS, and carcinogenic metabolites generate excessive oxidative stress, which changes the basal cellular status and leads to epigenetic modification, genomic instability, and initiation of cancer. Epigenetic modification may inhibit tumor-suppressor genes and activate oncogenes, enabling cells to have cancer promoting properties. The nuclear factor erythroid 2-related factor 2 (Nrf2) is a transcription factor that in humans is encoded by the NFE2L2 gene, and is activated in response to cellular stress. It can regulate redox homoeostasis by expressing several cytoprotective enzymes, including NADPH quinine oxidoreductase, heme oxygenase-1, UDP-glucuronosyltransferase, glutathione peroxidase, glutathione-S-transferase, etc. There is accumulating evidence supporting the idea that dietary nutraceuticals derived from commonly used fruits, vegetables, and spices have the ability to produce cancer chemopreventive activity by inducing Nrf2-mediated detoxifying enzymes. In this review, we discuss the importance of these nutraceuticals in cancer chemoprevention and summarize the role of dietary terpenoids in this respect. This approach was taken to accumulate the mechanistic function of these terpenoids to develop a comprehensive understanding of their direct and indirect roles in modulating the Keap1-Nrf2-ARE signaling system.

Abstract Dietary polyphenols have been widely investigated as antidiabetic agents in cell, animals, human study, and clinical trial. The number of publication (Indexed by Web of Science) on “polyphenols and diabetes” significantly increased since 2010. This review highlights the advances and opportunities of dietary polyphenols as antidiabetic agents. Dietary polyphenols prevent and manage Type 2 diabetes mellitus via the insulin‐dependent approaches, for instance, protection of pancreatic islet β‐cell, reduction of β‐cell apoptosis, promotion of β‐cell proliferation, attenuation of oxidative stress, activation of insulin signaling, and stimulation of pancreas to secrete insulin, as well as the insulin‐independent approaches including inhibition of glucose absorption, inhibition of digestive enzymes, regulation of intestinal microbiota, modification of inflammation response, and inhibition of the formation of advanced glycation end products. Moreover, dietary polyphenols ameliorate diabetic complications, such as vascular dysfunction, nephropathy, retinopathy, neuropathy, cardiomyopathy, coronary diseases, renal failure, and so on. The structure–activity relationship of polyphenols as antidiabetic agents is still not clear. The individual flavonoid or isoflavone has no therapeutic effect on diabetic patients, although the clinical data are very limited. Resveratrol, curcumin, and anthocyanins showed antidiabetic activity in human study. How hyperglycemia influences the bioavailability and bioactivity of dietary polyphenols is not well understood. An understanding of how diabetes alters the bioavailability and bioactivity of dietary polyphenols will lead to an improvement in their benefits and clinical outcomes.