Background. The relationship between diabetes and periodontitis is bidirectional, and there is now consensus that periodontitis and diabetes are comorbid. There is a quest for a drug that can be used to treat both conditions simultaneously. This study evaluated the anti-inflammatory and osteoprotective effects of liraglutide (LIRA) on periodontitis in diabetic rats. Methods. Male Wistar rats ( ) were randomly divided into four groups: control group ( ), LIRA group ( ), diabetes-associated periodontitis+0.9% saline group (diabetic periodontitis (DP)+NaCl group, ), and diabetes-associated periodontitis+LIRA group (DP+LIRA group, ). LIRA treatment lasted for 4 weeks (300 μg/kg/d) after establishment of a rat model of DP. The expression of IL-6, TNF-α, and IL-1β was detected by enzyme-linked immunosorbent assay. The morphological changes of periodontal tissues were observed by hematoxylin–eosin staining. The absorption of alveolar bone and its ultrastructural changes were observed by histomorphometry and microcomputed tomography. The expression of receptor activator of NF-κB ligand (RANKL) and osteoprotegerin (OPG) in alveolar bone was detected by immunohistochemistry. The levels of Runx2 mRNA and ALP mRNA in the gingival epithelium were examined by quantitative real-time polymerase chain reaction. Results. LIRA decreased alveolar bone resorption, improved the microstructure of alveolar bone, and reduced periodontal inflammation and damage ( ). LIRA also reduced blood glucose level and inhibited the secretion of serum IL-6, TNF-α, and IL-1β ( ). In addition, after treatment with LIRA, the ratio of RANKL/OPG was reduced, and the expression levels of ALP mRNA and Runx2 mRNA were upregulated ( ). Conclusions. LIRA not only controls blood glucose level but also reduces inflammation and bone loss and enhances osteogenic differentiation in diabetes-associated periodontitis. Those indicate that LIRA may be used as a potential medicine for the adjunctive therapy of diabetes-periodontitis comorbidity.

Diabetes and periodontitis exhibit a bidirectional relationship, posing significant challenges for the treatment of periodontitis in patients with diabetes. Our previous studies showed that the hypoglycemic agent liraglutide (LIRA), together with glycemic control, had favorable therapeutic effects on diabetic periodontitis (DP), achieving a “two birds with one stone” effect. Therefore, exploration of the topical application of LIRA for treating DP is warranted. In this study, nanoparticles were loaded with LIRA using poly (lactic-co-glycolic acid) (PLGA), and their morphology, particle size, encapsulation efficiency, drug loading, and drug release profiles were characterized. These nanoparticles were further encapsulated with hyaluronic acid (HA) to form a LIRA@PLGA/HA sustained-release system. The cytotoxicity of LIRA@PLGA/HA was analyzed using CCK-8 assays, and its anti-inflammatory and osteogenic effects on periodontitis in diabetic rats were evaluated by histology, ELISA, and micro-CT analysis, while its influence on necroptosis-related factors was assessed using qRT-PCR and Western blotting. The results indicated that LIRA@PLGA (30000 Da) exhibited an encapsulation efficiency of 86.2 %, a drug loading capacity of 4.3 %, and a cumulative release of LIRA reaching approximately 60 % after 8 days, thereby meting the requirement for sustained release. Following 24 h of stimulation with various concentrations (0–20 mg/ml) of LIRA@PLGA/HA, the viability of human periodontal ligament cells (HPDLCs) remained above 85 %. Topical application for four weeks significantly inhibited the expression of the inflammatory factors TNF-α and IL-1β in gingival crevicular fluid and serum, reduced inflammatory cell infiltration in periodontal tissues, and attenuated alveolar bone resorption while improving alveolar bone microstructure, showing therapeutic effects similar to the commercial drug PERIOCLINE® (PERIO). Furthermore, LIRA@PLGA/HA reduced the expression of necroptosis-related factors RIPK1, RIPK3, and MLKL. In conclusion, these results suggest that topical application of LIRA@PLGA/HA is effective for the treatment of DP through inhibition of necroptosis, representing a promising treatment strategy.

Since quinolone is a kind of synthetic broad-spectrum antibacterial drugs, with the widespread use of this class of antibiotics, the risk and harm to human health have been attendant to the sewage containing quinolones which are discharged into the environment. Photocatalysis is considered as a promising technology for antibiotic degradation for its strong redox properties and reaction rate. As a metal oxidizing substance, Bismuth vanadate (BiVO₄) is such a popular and hot material for the degradation of organic pollutants recently due to its good photocatalytic activity and chemical stability. Numerous studies have confirmed that BiVO₄ composites can overcome the shortcomings of pure BiVO₄ and cleave the main structure of quinolone under photocatalytic conditions. This paper mainly outlines the research progress on the preparation of BiVO₄ composites and the degradation of quinolone antibiotics from the perspective of improving the catalysis and degrading the efficiency mechanism of BiVO₄ composites.

Malignant melanoma, a rare and aggressive skin cancer, arises from the transformation of cutaneous melanocytes and is associated with a poor prognosis. Evodiamine (EVO), a bioactive compound derived from traditional Chinese herbal medicine, has demonstrated significant inhibitory effects on various tumor cells. In this study, we aimed to investigate the potential of EVO in regulating melanoma immunity and elucidate its underlying mechanisms. Experimental results revealed that the IC₅₀ value of EVO in B16-F10 cells for 24, 48, and 72 h were 11.73, 5.083, and 4.604 µM, respectively. EVO inhibited the proliferation, invasion, and metastasis of B16-F10 cells by more than 50%, while promoting apoptosis of higher concentration of EVO. EVO also significantly suppressed tumor growth by more than 80% and reduced spleen damage in tumor-bearing mice. Treatment with EVO led to a marked increase in T-cell subsets in the spleen, bone marrow, and tumors, with immunohistochemical (IHC) staining in particular showing about 50% higher. Furthermore, EVO inhibited the expression of programmed cell death ligand 1 (PD-L1) and the PI3K/AKT signaling pathway-related proteins in both B16-F10 cells and tumors. These findings suggest that EVO exerts antitumor effects by enhancing the tumor immune microenvironment and indicates its potential as a therapeutic agent for melanoma.