Biflavonoids, composed of two monoflavonoid residues, occur naturally in angiosperms, bryophytes, ferns, and gymnosperms. More than 592 biflavonoids have been structurally elucidated, and they can be classified into two groups of C-C and C-linear fragments-C, based on whether the linker between the two residues contains an atom. As the linker can be established on two arbitrary rings from different residues, the C-C type contains various subtypes, as does the C-linear fragment-C type. Biflavonoids have a wide range of pharmacological activities, including anti-inflammatory, antioxidant, antibacterial, antiviral, antidiabetic, antitumor, and cytotoxic properties, and they can be applied in Alzheimer’s disease and Parkinson’s disease. This review mainly summarizes the distribution and chemistry of biflavonoids; additionally, their bioactivities, pharmacokinetics, and synthesis are discussed.

Garcinia biflavonoid 1 (GB1) is one of the active chemical components of Garcinia kola and is reported to be capable of reducing the intracellular lipid deposition, which is the most significant characteristic of non-alcoholic fatty liver disease. However, its bioactive mechanism remains elusive. In the current study, the lipid deposition was induced in HepG2 cells by exposure to oleic acid and palmitic acid (OA&PA), then the effect of GB1 on lipid metabolism and oxidative stress and the role of regulating PPARα in these cells was investigated. We found that GB1 could ameliorate the lipid deposition by reducing triglycerides (TGs) and upregulate the expression of PPARα and SIRT6, suppressing the cell apoptosis by reducing the oxidative stress and the inflammatory factors of ROS, IL10, and TNFα. The mechanism study showed that GB1 had bioactivity in a PPARα-dependent manner based on its failing to improve the lipid deposition and oxidative stress in PPARα-deficient cells. The result revealed that GB1 had significant bioactivity on improving the lipid metabolism, and its potential primary action mechanism suggested that GB1 could be a potential candidate for management of non-alcoholic fatty liver disease.

Background: Attractive Toxic Sugar Baits (ATSBs) are an innovative vector control strategy based on the “attract-and-kill” principle. The core of ATSBs lies in the preparation of attractive and toxic baits through the mixing and proportioning of luring and active ingredients. Although previous studies have investigated the effects of ATSBs on mosquitoes, significant challenges remain for broader field application. Methods: This study evaluated five fruit juices as ATSBs for mosquitoes, focusing on feeding preferences. Preservative concentrations were assessed by measuring antimicrobial activity over time. Two commercial traps were tested for mosquito entry rates. The optimal insecticide species and concentration were determined based on mortality rates. An optimized ATSBs system was developed and tested under a semi-field cage. Statistical analysis was performed using GraphPad Prism. Results: Within 24 h, apple juice-based ATSBs had the highest attractant index for Culex quinquefasciatus and Anopheles sinensis, while a pear juice-based ATSB was most effective for Aedes albopictus. A 0.1% preservative concentration best maintained juice stability. The LC50 values of dinotefuran-based ATSBs for Cx. quinquefasciatus, Ae. albopictus, and An. sinensis were 1.18 × 10⁻³, 4.06 × 10⁻⁴, and 5.20 × 10⁻⁵ g/L, respectively. The Spodoptera frugiperda trap outperformed the Drosophilidae trap. Simulated semi-field cage tests showed 48 h mortality rates of 86.00% for Cx. quinquefasciatus and 95.67% for Ae. albopictus. Conclusion: This study optimized an ATSB system by screening various fruit juices, preservative concentrations, insecticides, and trap devices. The system’s efficacy in mosquito control was evaluated under a semi-field cage. These findings provide a strong foundation for the future application and refinement of ATSB-based mosquito control strategies.

Graphical GB1a attenuates DSS-induced ulcerative colitis via remodeling of the NF-κB and Nrf2 signaling pathways.