Hashimoto's thyroiditis (HT) is the most common organ‑specific autoimmune disease and is believed to be a predominately T cell‑mediated autoimmunity. Signal transducer and activator of transcription (STAT)3 is a crucial transcription factor of T cell‑mediated immunity, with key roles in the proliferation and migration of T helper (Th) cells, differentiation of Th cells into Th17 cells, and the balance between Treg cells and Th17 cells. Flavonoid luteolin has been shown to markedly inhibit Tyr705 activation/phosphorylation of STAT3 and exert anti‑inflammatory effects in multiple sclerosis. In the present study, the effect of luteolin on experimental autoimmune thyroiditis (EAT) was analyzed in C57BL/6 mice. Hematoxylin and eosin examination showed that luteolin attenuated lymphocytic infiltration and follicle destruction in thyroid glands. Immunohistochemistry results demonstrated that luteolin significantly reduced the phosphorylation of STAT3 within the thyroid. An in vitro study was carried out in a RAW264.7 macrophage cell line. Western blot findings demonstrated that luteolin significantly inhibited interferon‑γ‑induced increases in cyclooxygenase 2, phosphorylated STAT1 and phosphorylated STAT3 expression levels and the secretion of the proinflammatory cytokine tumor necrosis factor‑α in supernatants. The present findings indicated that luteolin may exert potent anti‑inflammatory effects on murine EAT, which may provide a novel therapeutic medication strategy for the early intervention of HT.

Background: Periodontitis is considered a risk factor for atherosclerosis, but the mechanism is not clear. It was reported that oral administration of Porphyromonas gingivalis altered the gut microbiota in mice. Gut dysbiosis and the intestinal metabolite trimethylamine N-oxide (TMAO) were verified to be associated with atherosclerosis. Therefore, the possible TMAO-related mechanism between periodontitis and atherosclerosis needs to be explored.Methods: Experimental periodontitis was established by oral administration of P. gingivalis for 2 months in ApoE^−/− mice. Mouse hemi-mandibles were scanned using Micro-CT. Quantification of TMAO was performed using liquid chromatography–tandem mass spectrometry. Mouse feces were collected and the bacterial DNA was extracted, then the gut microbiota was analyzed using 16S rRNA genes. Atherosclerotic lesion areas were quantified. Livers, small intestines, and large intestines were analyzed for gene expression.Results: Aggravated atherosclerosis plaques were found in experimental periodontitis mice. Plasma TMAO, a pathogenic factor of atherosclerosis, was initially found to be increased in periodontitis mice. Changes in the composition and abundance of the intestinal microflora of periodontitis mice were found. Flavin monooxygenase 3 (FMO3), the catalyzing enzyme of TMAO in the liver, was significantly increased, accompanied by an increase of IL-6 in liver, the abnormal intestinal integrity and enhanced plasma LPS. The IL-6 and LPS were verified to be able to increase FMO3 in HepG2 cells.Conclusion: Our research discovered that experimental periodontitis in ApoE^−/− mice induced gut dysbiosis and an increase in TMAO. These results suggest a possible mechanism by which periodontitis may accelerate atherosclerosis by influencing the intestinal microbes and the metabolism, which were triggered by inflammation of the liver and intestine.

Heme oxygenase-1 (HO-1), a stress-inducible protein with a potential anti-inflammatory effect, plays an important role in skin injury and wound healing. However, the function of HO-1 in cutaneous inflammatory diseases, such as psoriasis, remains unknown. The abnormal activation of Stat3, a known transcription factor that induces inflammation and regulates cell differentiation, is directly involved in the pathogenesis and development of psoriasis. Hence, targeting Stat3 is potentially beneficial in the treatment of psoriasis. In this study, HO-1 activation significantly alleviated the disease-related pathogenesis abnormality. To determine the mechanism by which HO-1 exerts immune protection on Th17-related cytokines, IL6/IL22-induced Stat3 activation was significantly suppressed, accompanied by decreased cell proliferation and reversed abnormal cell proliferation. Importantly, HO-1-induced Stat3 suppression was mediated through the activation of protein tyrosine phosphatase SHP-1. Overall, our study provides direct evidence indicating that HO-1 might be a useful therapeutic target for psoriasis. SHP-1-mediated suppression of Stat3 activation after HO-1 activation is a unique molecular mechanism for the regulation of Stat3 activation.

We aimed to design a novel three-dimensional (3D) printed surgical guide and evaluate its accuracy in assisting endodontic microsurgeries. A new 3D printed surgical guide was designed by computer-aided design and computer-aided manufacturing (CAD/CAM) technology and applied to 7 patients who underwent endodontic microsurgeries of upper anterior teeth from 2020.01 to 2020.12 as the experimental group. 7 patients who suffered from endodontic microsurgeries operated by the same surgeon without using the surgical guide from 2019.01 to 2019.12 were selected as the control group. Cone beam computed tomography (CBCT) was performed more than 12 months after operation, and the accuracy of apical resection was compared between the two groups. The accuracy of the microsurgery focused on the length and angle of the root apical resection. In the study, CBCT data and oral digital scanning data were used to reconstruct 3D models of periapical lesions with soft and hard tissue information, based on which we designed the new 3D printed surgical guides. The guides were successfully applied to the apectomy in endodontic microsurgeries. The deviation of the apical resection length of the experimental group (0.467 ± 0.146 mm) was better than that of the control group (1.743 ± 0.122 mm) (P < 0.0001), and the deviation of the apical resection angle of the experimental group (9.711 ± 3.593°) was significantly less than that of the control group (22.400 ± 3.362°) (P < 0.0001). The 3D-printed surgical guide could effectively guide endodontic microsurgery and improve its accuracy by fixing both the position and the angle of apectomy. The new type of surgical guide could accurately localize the root apex and guide the apical resection.