Opeyemi Joshua Olatunji

Soy peptides (SPs) have been extensively studied with an emphasis on their immune‐boosting effects and production‐associated bitterness. This associated bitterness affects SPs’ oral consumption despite their bioactivities. In this review, the immune‐boosting functions, factors affecting bitterness, and consumers’ perceptions of SPs are explored. Debittering/masking strategies to improve SP acceptability for oral consumption and formulation of SP‐based food products are ultimately provided. It is established that SPs can contribute to immune functions despite different factors affecting bitterness perception by consumers, ranging from dietary and culinary to genetic and other components of the food matrix. Furthermore, SP bitterness levels can be reduced using a wide range of biophysicochemical debittering and masking methods. This review provides a unique and integrative perspective by linking the immune‐boosting functions of SPs directly to the critical challenge of bitterness and its mitigation. Future studies focusing on highly efficient debittering techniques that support the immune‐boosting effect, quality, and mouthfeel of SPs and SP‐incorporated products are warranted.

Chinese ginger (Boesenbergia rotunda) is a culinary and traditional medicinal plant in Southeast Asia and Indo-China regions with several medicinal benefits. This study aims to assess the effectiveness of Chinese ginger extract against diabetic nephropathy and cardiomyopathy and the associated signaling pathways. Animals were randomly assigned to groups; control rats, diabetic rats, diabetic rats treated with 100 and 400 mg/kg of the B. rotunda EtOAc fraction (BRE). Treatment was administered for 5 successive weeks via oral gavage. Thereafter, the rats were evaluated for fasting blood glucose, tumour necrosis factor alpha, interleukin-6, interleukin-1 beta, reduced glutathione, superoxide dismutase, catalase, lipid peroxidation activities. Gene expression levels of nuclear factor erythroid 2-related factor 2, and Kelch-like ECH-associated protein 1 were examined. Cardiorenal histopathological and immunohistochemical were performed to assess tissue damage. BRE administration to diabetic rats notably ameliorated changes in body weight, kidney and heart weight and fasting blood glucose level. Furthermore, in diabetic rats, BRE significantly reduced malonaldehyde, tumour necrosis factor alpha, interleukin-6, interleukin-1 beta levels considerably with increasing activity of antioxidant enzymes in the kidney and cardiac tissues of rats treated with BRE. Diabetic rats treated with BRE showed upregulated mRNA expression levels of nuclear factor erythroid 2-related factor 2, while Kelch-like ECH-associated protein 1 mRNA expression in the kidney and cardiac tissues were downregulated. In addition, BRE treatment significantly reduced the cardiorenal protein expression of Bcl2 and collagen IV in the immunohistochemical analyses. From the results of this study, it can be concluded that B. rotunda exerts cardiorenal protective effect on diabetic rats due to its antidiabetic and antioxidant and may be considered a treatment for T2DM.

The herbal formula Qing-Luo-Yin (QLY) shows potential in activating PPARγ. This study investigated how this property contributed to its anti-rheumatic effects. Some mice with antigen-induced arthritis (AA) were orally treated with QLY and/or PPARγ antagonist/agonist (T0070907/rosiglitazone). PPARγ agonists were screened out by molecular docking and validated by experiments in vitro. Rosiglitazone and QLY ameliorated arthritis, inflammation and lipid depletion of AA mice. The effects of QLY were weakened by T0070907. Among the compounds abundant in QLY extract and QLY-treated adjuvant-induced arthritis (AIA) rats' serum, matrine, sophocarpine and sinomenine exhibited high affinities to PPARγ, and elevated its thermal stability and transcriptional activity. They suppressed fat utilisation in AIA serum-incubated HepG2 hepatocytes. Accumulated fatty acids in the medium reduced TNF-ɑ, IL-6 and IL-1β secretion of lipopolysaccharide-stimulated THP-1 monocytes by inhibiting p65 phosphorylation. In short, certain alkaloids in QLY activate PPARγ signalling, which contributes to the improvements of both immune and metabolic environments.

Mediterranean seaweeds are a valuable source of bioactive compounds that evolved in response to the region's unique conditions. These compounds, initially serving defensive roles, show strong pharmaceutical potential with antimicrobial, antioxidant, anti-inflammatory, antiviral, and anticancer properties. Rich in polysaccharides, polyphenols, and essential fatty acids, these macroalgae are increasingly recognized for their role in functional foods and nutraceuticals. However, research gaps persist, especially in chemical characterization and microbial profiling. The diversity, ecological roles, metabolic capabilities, and nutraceutical potential of the associated microorganisms are still poorly understood. This review offers an overview of the chemical and microbial profiling of Mediterranean seaweeds, emphasizing their pharmacological and nutraceutical value. It highlights the role of symbiotic microorganisms in metabolite biosynthesis and explores strategies to enhance the production of bioactive compounds. By doing so, this review aims to unlock the full potential of Mediterranean seaweeds and their microbial partners for sustainable pharmaceutical, nutraceutical, and industrial applications.

The rhizome of Dioscorea spongiosa is used in Chinese herbal medicine as Bixie (BX), a drug with antirheumatic effects. To explore the mechanisms underlying its antiangiogenic actions, adjuvant-induced arthritis (AIA) rats were administered with BX extract for 28 days. The therapeutic efficacy was evaluated by serological, histological, and immunohistochemical tests. Metabolites were quantified by kits and UPLC-MS. The BX extract was separated into 30 fractions by silica gel chromatography. The antiangiogenic effects of reagents were assessed based on wound-healing, migration, and tube-formation experiments using human umbilical vein endothelial cells (HUVECs). Protein targets were pulled down by a biotin-conjugated compound. These proteins and constituents in BX-related samples were identified by LC-MS. The target was validated by molecular simulation, immunoprecipitation, thermal shift assays, and enzymatic digestion. BX mitigated the metabolic abnormalities, inflammation, and synovial invasion of AIA rats. Angiogenesis in white adipose tissues and joints was suppressed, shown by the decrease of vessels, angiogenic cytokines, and CD31. The BX extract inhibited glycolysis and angiogenic capabilities of HUVECs. The expression of some genes/proteins related to VEGF and glycolytic signals was reduced. Diosgenin was the only component with high concentrations in the two most effective fractions and a BX-treated rat's serum. It curbed the glycolysis-fueled activation of HUVECs. Diosgenin competed with biotin-diosgenin when bound to ROCK1. It stabilized ROCK1 and inhibited ROCK1 phosphorylation. Its effects on VEGF-treated cells were similar to GSK429286 (a ROCK1 inhibitor) and weakened by arachidonate (a ROCK1 activator). It hardly affected ROCK1-silenced HUVECs. In short, diosgenin inhibits ROCK1 and suppresses angiogenesis via glycolysis downregulation.