High expression of ARHI inhibited the expression of MDR1 in Hela and Hela-TR cells. The cell viability and cell clone of Hela and Hela-TR cells were decreased by ARHI overexpression but increased by ARHI suppression. In addition, highly expressed ARHI promoted apoptosis and activated autophagy by increasing LC3-II/LC3-I through inactivating AKT/mTOR signaling pathway. In conclusion, overexpression of ARHI can increase the sensitivity of CC to paclitaxel through promoting apoptosis and autophagy in a AKT/mTOR inactivation dependent pathway.To investigate the role of loganin in hypoxia/reperfusion (H/R)-induced renal tubular epithelial cells and ischemia/reperfusion-induced acute kidney injury (AKI). Cells were received H/R treatment and cultured with different concentrations of loganin. The cell activity and apoptosis were detected. The expressions of apoptosis-related proteins, inflammatory factors, oxidative stress related molecules, and related molecules of JAK2/STAT3 and Nrf2/HO-1 signaling pathways were measured. AKI model of mice was established by I/R procedure, and the kidney was collected for hematoxylin and eosin (HE) staining. H/R treatment inhibited cell activity and apoptosis, but loganin attenuated the effect of H/R. Moreover, loganin inhibited H/R-induced inflammatory response and oxidative stress in tubular epithelial cells. Loganin down-regulated the expression of apoptosis-related proteins, suppressed JAK2/STAT3 pathway, and activated Nrf2/HO-1 pathway. In animal experiment, loganin reduced tubular injury in AKI mice.Loganin had anti-apoptotic, anti-inflammatory, and anti-oxidative stress effects on H/R-induced tubular epithelial cells, and could improve AKI in mice induced by I/R. This effect might be achieved by inhibiting JAK2/STAT3 and activating the Nrf2/HO-1 signaling pathway. To identify invasive dental procedures as a risk factor for postoperative spinal infection (PSI) and evaluate the effectiveness of antibiotic prophylaxis. We analysed 229,335 patients who underwent spinal surgery with instrumentation from 2010 to 2017, using the nationwide database. The incidence of spinal infection 2 years after surgery was determined. Invasive dental procedures as a risk factor for PSI and the effects of antibiotic prophylaxis during this period were also analysed. A total of 15,346 patients (6.69%) were diagnosed with PSI. It was found that advanced age, male sex, and a high Charlson Comorbidity Index were risk factors for PSI. The risk of PSI did not increase following dental procedures (adjusted hazard ratio [HR] 0.850; 95% confidence interval [CI], 0.793-0.912) and was not affected by antibiotics (adjusted HR 1.097; 95% CI, 0.987-1.218). Patients who received dental treatment as early as 3months after spinal surgery had the lowest risk of postoperative infection (adjusted HR 0.869; 95% CI, 0.795-0.950). Invasive dental procedure does not increase the risk of PSI, and antibiotic prophylaxis before dental procedure was not effective in preventing spinal infection. Invasive dental procedure does not increase the risk of PSI, and antibiotic prophylaxis before dental procedure was not effective in preventing spinal infection.In mammals, oocytes are arrested at G2/prophase for a long time, which is called germinal vesicle (GV) arrest. After puberty, fully-grown oocytes are stimulated by a gonadotropin surge to resume meiosis as indicated by GV breakdown (GVBD). CCNB1 is accumulated to a threshold level to trigger the activation of maturation promoting factor (MPF), inducing the G2/M transition. It is generally recognized that the anaphase-promoting complex/cyclosome (APC/C) and its cofactor CDH1 (also known as FZR1) regulates the accumulation/degradation of CCNB1. Here, by using small interfering RNA (siRNA) and messenger RNA (mRNA) microinjection, immunofluorescence and confocal microscopy, immunoprecipitation, time-lapse live imaging, and immunoblotting analysis, we showed that Septin 4 regulates the G2/M transition by regulating the accumulation of CCNB1 via APC/CCDC20 . Depletion of Septin 4 caused GV arrest by reducing CCNB1 accumulation. Unexpectedly, the expression level of CDC20 was higher in Septin 4 siRNA-injected oocytes than in control oocytes, but there was no significant change in the expression level of CDH1. Importantly, the reduced GVBD after Septin 4 depletion could be rescued not only by over-expressing CCNB1 but also could be partially rescued by depleting CDC20. Taken together, our results demonstrate that Septin 4 may play a critical role in meiotic G2/M transition by indirect regulation of CCNB1 stabilization in mouse oocytes.Immunocytes-involved inflammation is considered to modulate the damage in various diseases. https://www.selleckchem.com/products/kynurenic-acid.html Oxidative stress is initiated by oxidative agents such as LPS and ROS, which are strongly involved in chronic inflammation. Our previous study found that a polysaccharide fraction from Craterellus cornucopioides (CCPP-1) showed good antioxidant activity. However, the anti-inflammatory effect of CCPP-1 was still elusive. The objective of this study was to evaluate the anti-inflammatory activity of CCPP-1 and its potential mechanism in LPS-stimulated RAW264.7 macrophages. The results showed that CCPP-1 could inhibit LPS-induced ROS and NO accumulation. Additionally, CCPP-1 could decrease pro-inflammatory cytokines production (TNF-α, IL-1β, and IL-18) and inflammatory mediator (iNOS) expression, which might be associated with its capacity to inhibit NF-κB signaling pathway and NLRP3 inflammasome activation. Therefore, this study suggested that CCPP-1 had an ameliorative effect on the inflammation response and was potential to develop into functional food for treating chronic inflammation. PRACTICAL APPLICATIONS Craterellus cornucopioides is an edible fungus widely distributed in Southwestern China. It was reported that C. cornucopioides polysaccharide (CCPP-1), as important active ingredient, showed good antioxidant activity. However, the anti-inflammatory effect was still elusive. This study showed that CCPP-1 possessed anti-inflammatory activity. The molecular mechanism might be associated with its capacity to inhibit NF-κB signaling pathway and NLRP3 inflammasome activation. Therefore, polysaccharides from C. cornucopioides have potential to develop into functional food to combat inflammatory condition and thus indirectly halt the progression of various inflammatory response-related chronic diseases.