Oxidative stress refers to an imbalance between oxidative capacity and antioxidant capacity, leading to oxidative damage to proteins, lipids, and DNA, which can result in cell senescence or death. It is closely associated with the occurrence and development of various diseases, including cardiovascular diseases, nephropathy, malignant tumors, neurodegenerative diseases, hypertension, diabetes, and inflammatory diseases. Curcumin is a natural polyphenol compound of β-diketone, which has a wide range of pharmacological activities such as anti-inflammatory, antibacterial, anti-oxidative stress, anti-tumor, anti-fibrosis, and hypolipidemic, demonstrating broad research and development value. It has a wide range of biological targets and can bind to various endogenous biomolecules. Additionally, it maintains the redox balance primarily by scavenging ROS, enhancing the activity of antioxidant enzymes, inhibiting lipid peroxidation, and chelating metal ions. This paper systematically describes the antioxidative stress mechanisms of curcumin from the perspective of signaling pathways, focusing on the Keap1-Nrf2/ARE, NF-κB, NOX, MAPK and other pathways. The study also discusses potential pathway targets and the complex crosstalk among these pathways, aiming to provide insights for further research on curcumin’s antioxidant mechanisms and its clinical applications.

1,3,6-Trigalloylglucose is a natural compound that can be extracted from the aqueous extracts of ripe fruit of Terminalia chebula Retz, commonly known as “Haritaki”. The potential anti-Helicobacter pylori (HP) activity of this compound has not been extensively studied or confirmed in scientific research. This compound was isolated using a semi-preparative liquid chromatography (LC) system and identified through Ultra-high-performance liquid chromatography–MS/MS (UPLC-MS/MS) and Nuclear Magnetic Resonance (NMR). Its role was evaluated using Minimum inhibitory concentration (MIC) assay and minimum bactericidal concentration (MBC) assay, scanning electron microscope (SEM), inhibiting kinetics curves, urea fast test, Cell Counting Kit-8 (CCK-8) assay, Western blot, and Griess Reagent System. Results showed that this compound effectively inhibits the growth of HP strain ATCC 700392, damages the HP structure, and suppresses the Cytotoxin-associated gene A (Cag A) protein, a crucial factor in HP infection. Importantly, it exhibits selective antimicrobial activity without impacting normal epithelial cells GES-1. In vitro studies have revealed that 1,3,6-Trigalloylglucose acts as an anti-adhesive agent, disrupting the adhesion of HP to host cells, a critical step in HP infection. These findings underscore the potential of 1,3,6-Trigalloylglucose as a targeted therapeutic agent against HP infections.

Background: Terminalia chebula Retz, known as the King of Tibet, is considered a functional food in China, celebrated for its antioxidant, immune-modulating, antibacterial, and anti-inflammatory properties. Chebulinic acid, derived from aqueous extracts of Terminalia chebula Retz, is known for its anti-inflammatory properties. However, its potential as an anti-Helicobacter pylori (HP) agent has not been fully explored.Methods: Herein, we extracted the main compound from Terminalia chebula Retz using a semi-preparative liquid chromatography (LC) system and identified compound 5 as chebulinic acid through Ultra-high performance liquid chromatography-MS/MS (UPLC–MS/MS) and Nuclear Magnetic Resonance (NMR). To evaluate its role, we conducted minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) assays, scanning electron microscope (SEM) imaging, inhibiting kinetics curves, urea fast test, cell counting kit-8 (CCK-8) assay, western blot analysis, griess reagent system, and molecular docking.Results: Our results showed that chebulinic acid effectively inhibited the growth of the HP strain ATCC 700392, damaged the HP structure, and exhibited selective antimicrobial activity without affecting normal epithelial cells GES-1. Importantly, it suppressed the expression of Cytotoxin-associated gene A (Cag A) protein, a crucial factor in HP infection. Molecular docking analysis predicted a strong affinity (−9.7 kcal/mol) between chebulinic acid and Cag A protein.Conclusion: Overall, our findings suggest that chebulinic acid acts as an anti-adhesive agent, disrupting the adhesion of HP to host cells, which is a critical step in HP infection. It also suppresses the Cag A protein. These results highlight the potential of chebulinic acid against HP infections.

As a type of transdermal drug delivery system (TDDS), Microneedles (MNs) have garnered significant attention from researchers due to their ability to penetrate the stratum corneum (SC) of the skin, enhance drug permeability and bioavailability, avoid first-pass metabolism, and cause minimal damage to the skin. This makes them particularly suitable for localized transdermal drug delivery. Dissolvable microneedles (DMNs) can encapsulate sensitive particles, provide high drug-loading capacity, and possess biodegradability and biocompatibility, attracting extensive research interest. Chitosan (CS) has been selected as the matrix for manufacturing DMNs due to its excellent properties, including not eliciting an immune response in vivo and having active functional groups such as hydroxyl and amino groups that allow for modifications to impart appropriate mechanical strength and functionality to DMNs for specific applications. This paper provides a comprehensive review of the research status of various chitosan-based microneedles (CSMNs), explores the mechanisms of their dissolution in vivo, and discusses their applications in promoting wound healing, delivering macromolecular drugs, vaccine delivery, and anti-tumor therapies.