Vein graft (VG) failure (VGF) is associated with VG intimal hyperplasia, which is characterized by abnormal accumulation of vascular smooth muscle cells (VSMCs). Most neointimal VSMCs are derived from pre-existing VSMCs via a process of VSMC phenotypic transition, also known as dedifferentiation. There is increasing evidence to suggest that ginger or its bioactive ingredients may block VSMC dedifferentiation, exerting vasoprotective functions; however, the precise mechanisms have not been fully characterized. Therefore, we investigated the effect of ginger on VSMC phenotypic transition in VG remodeling after transplantation. Ginger significantly inhibited neointimal hyperplasia and promoted lumen (L) opening in a 3-month VG, which was primarily achieved by reducing ferroptotic stress. Ferroptotic stress is a pro-ferroptotic state. Contractile VSMCs did not die but instead gained a proliferative capacity and switched to the secretory type, forming neointima (NI) after vein transplantation. Ginger and its two main vasoprotective ingredients (6-gingerol and 6-shogaol) inhibit VSMC dedifferentiation by reducing ferroptotic stress. Network pharmacology analysis revealed that 6-gingerol inhibits ferroptotic stress by targeting P53, while 6-shogaol inhibits ferroptotic stress by targeting 5-lipoxygenase (Alox5), both promoting ferroptosis. Furthermore, both ingredients co-target peroxisome proliferator-activated receptor gamma (PPARγ), decreasing PPARγ-mediated nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 1 (Nox1) expression. Nox1 promotes intracellular reactive oxygen species (ROS) production and directly induces VSMC dedifferentiation. In addition, Nox1 is a ferroptosis-promoting gene that encourages ferroptotic stress production, indirectly leading to VSMC dedifferentiation. Ginger, a natural multi-targeted ferroptotic stress inhibitor, finely and effectively prevents VSMC phenotypic transition and protects against venous injury remodeling.

RNAs are involved in the crucial processes of disease progression and have emerged as powerful therapeutic targets and diagnostic biomarkers. However, efficient delivery of therapeutic RNA to the targeted location and precise detection of RNA markers remains challenging. Recently, more and more attention has been paid to applying nucleic acid nanoassemblies in diagnosing and treating. Due to the flexibility and deformability of nucleic acids, the nanoassemblies could be fabricated with different shapes and structures. With hybridization, nucleic acid nanoassemblies, including DNA and RNA nanostructures, can be applied to enhance RNA therapeutics and diagnosis. This review briefly introduces the construction and properties of different nucleic acid nanoassemblies and their applications for RNA therapy and diagnosis and makes further prospects for their development.

Periodontitis is an inflammatory disease caused by bacterial infection directly, and the dysregulation of host immune-inflammatory response finally destroys periodontal tissues. Current treatment strategies for periodontitis mainly involve mechanical scaling/root planing (SRP), surgical procedures, and systemic or localized delivery of antimicrobial agents. However, SRP or surgical treatment alone has unsatisfactory long-term effects and is easy to relapse. In addition, the existing drugs for local periodontal therapy do not stay in the periodontal pocket long enough and have difficulties in maintaining a steady, effective concentration to obtain a therapeutic effect, and continuous administration always causes drug resistance. Many recent studies have shown that adding bio-functional materials and drug delivery systems upregulates the therapeutic effectiveness of periodontitis. This review focuses on the role of biomaterials in periodontitis treatment and presents an overview of antibacterial therapy, host modulatory therapy, periodontal regeneration, and multifunctional regulation of periodontitis therapy. Biomaterials provide advanced approaches for periodontal therapy, and it is foreseeable that further understanding and applications of biomaterials will promote the development of periodontal therapy.

Objective To synthesize novel gold nanoparticles of GAL-PEG-GNPs,study its radiation effect on hepatocellular carcinoma cells HepG2 cells in vitro,and investigate the underlying mechanisms.Methods GAL-PEG-GNPs were synthesized and characterized successfully.HepG2 cells were divided into three groups of control,GNPs and GAL-PEG-GNPs.The cytotoxicities of these compounds were tested by the CCK-8 assay and their IC50 values of HepG2 cells were calculated.Cell uptake of nanoparticles was detected by TEM and ICP-MS.The radiosensitization effect of nanoparticles was tested by the colony formation assay.Cell cycle distribution was detected by FCM.The expressions of CAT,SOD,and total GSH were detected with a microplate reader,and the expressions of apoptosis-related proteins were tested by Western blot.Results The GNPs and GAL-PEG-GNPs had absorption peaks at 520 and 530 nm,respectively,and their diameters were (22.6-±2.12) and (32.0 ± 1.41) nm detected by ICP-MS.The GAL-PEG-GNPs and GNPs had similar cytotoxicity profiles (P ＞ 0.05),while GAL-PEG-GNPs could be more effectively uptaken by HepG2 cells than GNPs.The sensitive enhancement ratio (SER) of GNPs and GAL-PEG-GNPs to HepG2 cells were 1.46 和 1.95,respectively.The percentage of cells at phase of G2/M in HepG2 population treated with GNP was higher than that of untreated cells (t =14.20,P ＜0.05).The protein expressions of Cytochrome C,Bax,Caspase-3,and Caspase-9 were upregulated while Bcl-2 expression was down-regulated in the cells treated with GNPs/radiation or GAL-PEGGNPs/radiation.The expressions of CAT,SOD and total GSH in the GNP treated groups were significantly decreased compared with the control group(t =12.34,29.39,12.85,P ＜ 0.05).Conclusions GALPEG-GNPs has obvious radiosensitization effect on HepG2 cells,which is related to the induction of cell apoptosis and the generation of free radicals.