Food and Humanity, Год журнала: 2024, Номер unknown, С. 100440 - 100440
Опубликована: Окт. 1, 2024
Язык: Английский
Food and Humanity, Год журнала: 2024, Номер unknown, С. 100440 - 100440
Опубликована: Окт. 1, 2024
Язык: Английский
Frontiers in Nutrition, Год журнала: 2025, Номер 12
Опубликована: Янв. 30, 2025
The antioxidant activity of natural products is closely related to their antiglycation effects. This study aimed examine the and elucidate underlying mechanisms two specific peptides, EDYGA (Glu-Asp-Tyr-Gly-Ala) DLLCIC (Asp-Leu-Leu-Cys-Ile-Val), derived from protein hydrolysates Pelodiscus sinensis . Both were efficient in bovine serum albumin (BSA)/glucose model inhibit BSA glycation, while showed higher than EDYGA. Firstly, it was found that could formation NEG AGEs. Moreover, able maintain secondary structure stabilize band positions (amide I & II). Additionally, molecular simulations indicated can spontaneously interact with central site BSA, specifically at Lys114 Glu424 residues, through hydrogen bonds an energy strength −0.7 kcal/mol. Furthermore, CCK-8 morphological experiments confirmed improved cell survival against AGEs-induced cytotoxicity, EC50 values 17.64 μM for 15.08 DLLCIC. These findings serve as a significant reference development effective agents prevention glycation-mediated diseases.
Язык: Английский
Процитировано
0Pharmacological Research, Год журнала: 2025, Номер unknown, С. 107754 - 107754
Опубликована: Апрель 1, 2025
Pyroptosis is a distinct form of cell death that plays critical role in intensifying inflammatory responses. It primarily occurs via the classical pathway, non-classical caspase-3/6/7/8/9-mediated pathways, and granzyme-mediated pathways. Key effector proteins involved pyroptosis process include gasdermin family pannexin-1 protein. intricately linked to onset progression non-alcoholic steatohepatitis (NASH). During development NASH, factors such as pyroptosis, innate immunity, lipotoxicity, endoplasmic reticulum stress, gut microbiota imbalance interact interweave, collectively driving disease progression. This review analyzes molecular mechanisms its pathogenesis NASH. Furthermore, it explores potential diagnostic therapeutic strategies targeting offering new avenues for improving diagnosis treatment
Язык: Английский
Процитировано
0Nutrients, Год журнала: 2024, Номер 16(23), С. 4208 - 4208
Опубликована: Дек. 5, 2024
Metabolic dysfunction-associated steatotic liver disease (MASLD) represents a refined categorization of non-alcoholic fatty (NAFLD), highlighting the intricate relationship between hepatic steatosis and metabolic dysfunction. Abdominal obesity (AO), key diagnostic criterion for dysfunction, predominantly results from inappropriate diet unhealthy dietary habits. To comprehensively investigate which factors contribute to MASLD through AO understand underlying biological mechanisms, we initially conducted systematic review meta-analysis articles in PubMed database past decade, summarizing that affect AO. Subsequently, targeted searches these provided narrative mechanisms how lead exacerbates MASLD. A characterized by excessive intake energy, carbohydrates, fructose, or ultra-processed foods (UPFs) is considered inappropriate. Inappropriate leads formation enhancing pathways such as de novo lipid synthesis (DNL) liver, insulin resistance (IR), gut-liver inflammation. Dietary interventions diets can effectively intervene improve The mechanism on abdominal fat deposition energy activation enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD-1) increase endocortisol secretion. Then, accumulation visceral facilitates rapid augmented flux free acids (FFAs) initiates series deleterious effects, including oxidative stress (OS), endoplasmic reticulum (ERS), protein kinase C (PKC) pathways, Additionally, FFAs may mediate hepatocellular damage action hormones. These exacerbate progression steatohepatitis (MASH) fibrosis. Furthermore, investigating other potential influence could offer new recommendations treatment guidelines
Язык: Английский
Процитировано
2Food and Humanity, Год журнала: 2024, Номер unknown, С. 100440 - 100440
Опубликована: Окт. 1, 2024
Язык: Английский
Процитировано
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