To Draw a Detailed Map for Maxillofacial Fast-Flow Vascular Diseases With the Combination of Color Doppler Ultrasound and Three-Dimensional Computed Tomography Angiography.

Vascular diseases, such as vascular malformations and hemangiomas, are often classified into "fast-flow" and "slow-flow" based on their internal blood velocity. Fast-flow vascular diseases of maxillofacial regions are a kind of complicated and dangerous pathological changes originating from or containing arteries, their treatment is often complex and different from disease to disease, and large amounts of intraoperative blood loss and poor operation field may cause side injury or other problems without a detailed map of the lesion. The authors use the combination of color Doppler ultrasound and three-dimensional computed tomography angiography to diagnose and classify 36 cases of maxillofacial fast-flow vascular diseases, from January 2018 to December 2022 presented in the authors' department. Three-dimensional computed tomography angiography can display the location, type, and blood supply of lesions, whereas color Doppler ultrasound has unique advantages in identifying some special lesions (such as the colorful images of orificium fistulaes and the "Yin-yang sign" of pseudoaneurysms), then projecting and marking them on the body surface, which greatly facilitate the surgical procedure. This cost-effective and noninvasive combination shows significant clinical application value.

Development of controlled-release antioxidant poly (lactic acid) bilayer active film with different distributions of α-tocopherol and its application in corn oil preservation.

The antioxidant poly (lactic acid) bilayer active films with a different distribution of α-tocopherol (TOC) in two layers (outer layer/inner layer: 0%/6%, 2%/4%, 3%/3%, 4%/2%, 6%/0%) were developed. The effects of TOC distribution on the structural, physicochemical, mechanical, antioxidant and release properties of the films and their application in corn oil packaging were investigated. The different distributions of TOC showed insignificant effects on the color, transparency, tensile strength and oxygen and water vapor barrier properties of the films, but it affected the release behavior of TOC from the films into 95% ethanol and the oxidation degree of corn oil. The film with higher TOC in outer layer showed a slower release rate. The corn oil packaged by the film containing 4% TOC in outer layer and 2% TOC in inner layer exhibited the best oxidative stability. This concept showed a great potential to develop controlled-release active films for food packaging.

Mechanisms of action underlying Shentong Zhuyu decoction based treatment of rheumatoid arthritis using systems biology and computer-aided drug design.

Rheumatoid arthritis is an autoimmune disease characterized by chronic polyarticular pain, for which no cure currently exists. In Chinese medicine, rheumatoid arthritis (RA) is believed to be caused by phlegm and blood stagnation. Shentong Zhuyu decoction can be used to treat RA, as it promotes blood circulation, resolves blood stasis, and relieves pain. In our study, we used network pharmacology and computer-aided drug design to evaluate the components, active compounds, and targets of Shentong Zhuyu decoction (STZY). Our results suggest that STZY contains active compounds such as quercetin, luteolin, and formononetin that regulate immune network targets. RA associated genes are enriched in pathways including those associated with nuclear factor kappa B, phosphatidylinositol-3-kinase/AKT, and hypoxia inducible factor 1 signaling. The main active compounds in STZY (quercetin and luteolin) were derived from Achyranthis Bidentatae Radix, Carthami Flos, licorice, Cyperi Rhizoma, and Myrrha and targeted the pro-inflammatory cytokines interleukin 2, interleukin 1 alpha, interleukin 1 beta, and interleukin 6. In addition, the compounds quercetin, luteolin, and formononetin in these herbs can target the anti-inflammatory cytokines interleukin 4 and interleukin 10. Our results suggest that STZY can balance the immune network, promote an anti-inflammatory environment, and reduce the clinical symptoms of RA. Based on the close relationship between inflammatory response and osteoclast formation, we hypothesized that STZY may inhibit inflammation and alleviate bone destruction in RA. Our findings indicate that STZY can treat RA through multiple components, targets, and pathways. This study may provide a reference for the clinical application of STZY in RA treatment.

Celastrol relieves myocardial infarction-induced cardiac fibrosis by inhibiting NLRP3 inflammasomes in rats.

BACKGROUND: Myocardial infarction (MI) triggers a strong inflammatory response mediating by NLRP3 inflammasome which is associated with cardiac fibrosis. The key players in this response are Interleukin (IL)-1 and IL-18, which are regulated by NLRP3 inflammasomes. Celastrol, a traditional Chinese medicine with strong anti-inflammatory activity, has recently reported as a cardioprotective agent. However, the mechanisms by which celastrol is cardioprotective in MI remain elusive. We hypothesized that Celastrol could reduce IL-1ß and IL-18 expression and ameliorate myocardial fibrosis after myocardial infarction in rats, improve poor heart remodeling, and preserve heart function. METHODS: Myocardial infarction (MI) was caused by ligating the left anterior descending of male SD rats. Celastrol (1 mg/kg) or saline was administered every other day for 4 weeks. Heart function and fibrosis were assessed. Inflammatory and fibrotic markers in the myocardia were evaluated with immunohistochemistry, western blot, and ELISA. Molecular docking was employed to predict Celastrol's binding to NLRP3 protein. The effects of Celastrol on the expression of NLRP3 inflammasome and myocardial fibrosis genes were then examined in vitro. RESULTS: Celastrol maintained the left ventricular fractional shortening (FS) and ejection fraction (EF). Fibrosis was significantly reduced in animals treated with 1 mg/kg Celastrol (15.17 ± 1.82%) relative to controls (29.88 ± 4.28%). Celastrol also significantly reduced the NLRP3, IL-18, and IL-1ß levels, together with macrophage and neutrophil infiltration in the myocardium. Molecular docking predicted that NLRP3 would bind tightly to Celastrol [Docking energy: -8.9 (kcal/mol)]. In vitro experiments showed reduced NLRP3 inflammasome and myocardial fibrosis-associated proteins expression in neonatal rat cardiac fibroblasts treated with Celastrol. CONCLUSIONS: In post-MI rats, Celastrol, a naturally occurring active ingredient, was able to reduce myocardial fibrosis and improve cardiac function, according to our study. These effects may result from inhibiting the NLRP3 inflammasome and attenuating the early inflammatory storm after MI, suggesting that Celastrol may be useful in treating acute MI.

Huangkui lianchang decoction attenuates experimental colitis by inhibiting the NF-κB pathway and autophagy.

Ulcerative colitis (UC) is a chronic inflammatory colorectal disease characterized by excessive mucosal immune response activation and dysfunction of autophagy in intestinal epithelial cells. Traditional herbal preparations, including the Huangkui lianchang decoction (HLD), are effective in UC clinical treatment in East Asia, but the underlying mechanism is unclear. This study evaluated the therapeutic effects and associated molecular mechanisms of HLD in UC in vivo and in vitro. A C57BL/6 UC mouse model was established using 2.5% dextran sulfate sodium. The effects of HLD on the colonic structure and inflammation in mice were evaluated using mesalazine as the control. The anti-inflammatory effects of HLD were assessed using disease activity index (DAI) scores, histological scores, enzyme-linked immunosorbent assay, immunohistochemistry, immunofluorescence, and western blotting. HLD displayed a protective effect in UC mice by reducing the DAI and colonic histological scores, as well as levels of inflammatory cytokines and NF-κB p65 in colonic tissues. NCM460 lipopolysaccharide-induced cells were administered drug serum-containing HLD (HLD-DS) to evaluate the protective effect against UC and the effect on autophagy. HLD-DS exhibited anti-inflammatory effects in NCM460 cells by reducing the levels of inflammatory cytokines and increasing interleukin 10 levels. HLD-DS reduced p-NF-κB p65, LC3II/I, and Beclin 1 expression, which suggested that HLD alleviated colitis by inhibiting the NF-κB pathway and autophagy. However, there was no crosstalk between the NF-κB pathway and autophagy. These findings confirmed that HLD was an effective herbal preparation for the treatment of UC.