Byrnehall2151

82, 95% CI = 1.11-2.98). Long-term DAPT had no superiority compared with MAPT. Aspirin plus clopidogrel comparing with aspirin and early initiating treatment time comparing with MAPT decreased stroke recurrence (RR = 0.74, 95% CI = 0.67-0.83; RR = 0.69, 95% CI = 0.61-0.78) and ischemic stroke recurrence ( RR = 0.71, 95% CI = 0.64-0.79; RR = 0.68, 95% CI = 0.59-0.77) but also increased major bleeding (RR = 1.70, 95% CI = 1.38-2.09; RR = 1.75, 95% CI = 1.07-2.85). DAPT reduced stroke and ischemic stroke recurrence in non-Asian group but only reduced ischemic stroke recurrence in Asian group. As stroke secondary prevention, short-term DAPT rather than long-term DAPT could be a better choice. Patients could benefit more from aspirin plus clopidogrel or given DAPT within 72 h after symptoms onset. Race may be a factor influencing the efficacy of DAPT.An increasing number of studies have demonstrated that phillygenin (PG) exerts anti-oxidant, anti-inflammatory and anti-cancer activities. However, the effects of PG on the proliferation and invasion in non-small cell lung cancer (NSCLC) cells have not been clarified. In this study, MTT assay and flow cytometry were conducted to investigate the effect of PG on proliferation and apoptosis of NSCLC cells in vitro, respectively. A xenograft model of A549 cell was established in nude mice to validate the in vitro findings. Western blot were performed to measure the expression of molecules involved in AMPK/ERK/NF-κB pathway. Results suggested that PG (50 or 100 μM) was significantly cytotoxic to A549 cells and SPC-A1 cells in vitro. PG treatment also inhibited the tumor growth of NSCLC cell mouse xenografts in vivo. These anti-proliferative and pro-apoptosis effects of PG were found to be regulated by the AMPK/ERK/NF-κB pathway. Consequently, PG suppressed proliferation and induced cell apoptosis in NSCLC cells. In conclusions, PG regulates AMPK/ERK/NF-κB axis in NSCLC cells, thereby inhibiting the proliferation and promoting the apoptosis of NSCLC cells.The aim of the present study was to examine changes in the expression and activity of P-glycoprotein (P-gp) in human hepatocellular carcinoma HepG2 cells after exposure to menthol, and their relationship to the cytotoxicity of and apoptotic responses to doxorubicin (DOX), a substrate of P-gp, in the cells. The expression of P-gp in HepG2 cells was significantly increased by menthol treatment. Intracellular accumulation of DOX in HepG2 cells was significantly lower in the menthol-treated group than in the control group, but this phenomenon was abolished in the presence of verapamil. Decreased cell viability by DOX was significantly attenuated by 24-h menthol treatment prior to DOX exposure, which coincided with the changes in mRNA expression of Bcl-xl and caspase-3. These results demonstrate that menthol causes hepatocellular carcinoma cells to acquire resistance to DOX by increasing its efflux through the upregulation of P-gp.Objective Intervertebral disc degeneration (IVDD) is very common in the elderly, so it is particularly important to find appropriate prevention or treatment. The aim of this study was to explore the effect of dexmedetomidine (DEX) on the degeneration of nucleus pulposus (NP) cells and its mechanism. Methods We established a mouse model of IVDD and cultured mouse NP cells and treated them with IL-1β and DEX. The effect of DEX on NP cells was determined by detecting the extracellular matrix of NP cells, changes in ROS levels and inflammatory mediators. LY294002, a PI3K inhibitor, is used to inhibit the activity of the PI3K/Akt signaling pathway. The effect of DEX on the PI3K/Akt signaling pathway was determined by studying the effects of DEX on PI3K/ Akt signaling pathway-related molecules and the effect of LY294002 on NP cells degeneration. DEX significantly increased the disc height index and attenuated IVDD in mice. Results DEX significantly inhibited the expression of MMP3/9 in NP cells, effectively inhibiting the degradation of extracellular matrix. In addition, oxidative stress levels and inflammatory levels in NP cells are also attenuated by DEX. ULK inhibitor The expression of PI3K, Akt and p-Akt was significantly increased in DEX-stimulated NP cells, indicating that DEX increased the activity of the PI3K/Akt signaling pathway. DEX promotes PI3K/Akt signaling pathway, inhibits oxidative stress and inflammatory of NP cells, thereby slowing the degeneration of NP cells. Conclusion DEX promotes PI3K/Akt signaling pathway, inhibits oxidative stress and inflammatory of NP cells, thereby slowing the degeneration of NP cells.The etiology of osteoarthritis (OA) has been discussed widely, but the molecular mechanisms beneath OA aggravation have not yet been investigated in detail. This study focused on the role of lncRNA RMRP (RMRP) on OA progression. We found that the expression of RMRP was significantly increased in cartilage tissues of patients with OA. CCK-8 and colony formation assays showed that RMRP knockdown promoted proliferation of chondrocytes treated with IL-1β. Flow cytometry and caspase-3 activity analysis indicated that RMRP silence inhibited apoptosis of chondrocytes treated with IL-1β. Moreover, luciferase reporter, RNA pull-down and RIP assays showed that RMRP competing with miR-206. Additionally, CDK9 acted as a direct target of miR-206. Moreover, rescue assays indicated that miR-206 inhibitor or pcDNA-CDK9 reversed the effects of RMRP suppression on the proliferation and apoptosis of chondrocytes. Taken together, our results indicated that RMRP knockdown could promote proliferation and inhibit apoptosis in OA chondrocytes via the miR-206/CDK9 axis.Platinum (Pt)-based drugs are routinely used to treat oral cancer (OC), but occurrence of therapeutic resistance remains a formidable challenge in cancer treatment. We sought to explore the cytotoxicity of non-classical Pt-based compounds, and compared the efficacy and anticancer activity of 56MESS with cisplatin in OC. Drug sensitivity of seven non-classical Pt-based compounds as well as cisplatin were determined by CCK-8 assay. Comparison of cytotoxic effects between 56MESS, phenanthriplatin and cisplatin was performed on six different OC cell lines. The anticancer effects of 56MESS was further measured both in vitro and in vivo. Additionally, the biological role of FACL4 and its relationship with 56MESS-induced growth inhibition were investigated. Two out of seven Pt-based compounds displayed a significant cytotoxic effect. 56MESS was chosen as the most potent compound due to its highly selective cytotoxic activity. 56MESS particularly caused G2/M phase arrest, while failed to induce apoptosis. In vivo, 56MESS had a higher cytotoxic capacity than cisplatin.