Sextonrafferty6220

TCM could protect COVID-19 patients from tissue injuries, a protection that might be, at least partially, attributed to the anti-inflammatory, antioxidant and anti-apoptotic effects of the TCM under investigation. This review provides evidence and support for clinical treatment and novel drug research using TCM.

TCM could protect COVID-19 patients from tissue injuries, a protection that might be, at least partially, attributed to the anti-inflammatory, antioxidant and anti-apoptotic effects of the TCM under investigation. This review provides evidence and support for clinical treatment and novel drug research using TCM.Syringic acid is an abundant phenolic acid compound that possesses anti-oxidant, anti-microbial, anti-inflammatory, and anti-endotoxic properties. However, the research of pretreatment with syringic acid against myocardial ischemia reperfusion is still limited. Thus, our research revealed the protective effect of syringic acid in the rat model with myocardial ischemia reperfusion injury. Histological analysis was performed by hematoxylin and eosin (H&E). The myocardial systolic function was detected by echocardiographic. Myocardial infarct size was measured by Evans blue and 2,3,5-triphenyltetrazolium chloride (TTC) double staining. The apoptosis index was recorded by Terminal deoxynucleotidyl transferase dUTP nick end labeling staining (TUNEL). The contents of creatine kinase MB (CK-MB) and lactate dehydrogenase (LDH) in the serum were determined by a commercial kit. The expression of the PI3K/Akt/GSK-3β signaling pathway-related molecules and apoptosis-associated indicators was detected by western blotting or real-time PCR. We found that pretreatment with syringic acid obviously increased the myocardial systolic function (LVEF and LVFS) and decreased the infarct size, the apoptosis index as well as the serum level of CK-MB and LDH. Meanwhile, syringic acid also remarkably augmented the contents of p-PI3K, p-Akt, p-GSK-3β, Bcl-2 and mitochondria cytochrome c. However, the expression of caspase-3, -9 and Bax significantly reduced. Interestingly, co-treatment with PI3K inhibitor of LY294002 counteracted those effects induced by syringic acid. In conclusion, pretreatment with syringic acid can mitigate myocardial ischemia reperfusion injury by inhibiting mitochondria-induced apoptosis which is regulated by the PI3K/Akt/GSK-3β signaling pathway.Activated hepatic stellate cells (HSCs) play a central role in fibrillary collagen production, the primary cause of liver fibrosis. Although it is known that primary cultured HSCs are activated by plastic culture dish stiffness, HSC activation and quiescent-state-reversion mechanisms are still unclear. In this study, we used cultured normal rat HSCs on 3.2 kPa collagen normal liver stiffness equivalent gel, to determine whether high glucose or high succinate conditions induce HSC activation, and examined whether activated HSCs reverted to a quiescent state when suppressed by GPR91 antagonists or TGF-β1 receptor inhibitors. We measured the gene expression levels of α-SMA and type I collagen HSC activation markers using real-time PCR. Our data indicated that high glucose conditions induced HSC activation, and showed that under continuous high glucose exposure HSC activation progressed. A GPR91 antagonist, 2 d, and a TGF-β1 receptor inhibitor, SB525334, suppressed the Col1α mRNA expression level of these activated HSCs. Similarly, under extended high succinate exposure, 2 d and SB525334 reduced Col1α mRNA expression levels of activated HSCs. From the above, we determined that even though HSCs had already been activated by high glucose or succinate conditions which persisted after activation, the GPR91 antagonist and the TGF-β1 receptor inhibitor were able to reduce the production of type I collagen from activated HSCs.Anaplastic thyroid carcinoma (ATC) is a rare and aggressive malignancy that accounts for the majority of deaths from all thyroid cancers. ATC exhibits invasiveness and highly resistance to conventional therapies which include cytotoxic chemotherapy, the combination of BRAF and MEK inhibition and, more recently, immunotherapies, that have shown promising but still limited results. read more A growing knowledge on ATC tumor biology is needed for developing more effective therapies with significant better survival. Researchers have begun to utilize 3D models to culture cancer cells for in vitro studies. In this work, C643 ATC cell line was cultured on polymeric scaffolds with high-interconnected porous matrix. They exhibited distinct viability, proliferation and 3D morphology similar to an in vivo solid tumor mass. We also carried out quantitative real-time PCR experiments for monitoring Cancer Stem Cells enrichment, since they are most probably the cause of tumor resistance, reoccurrence and metastasis. The same tests were performed after cell treatment with the chemotherapic Doxorubicin. An up-regulation of the analyzed stem-cell markers confirmed the high resistance to treatment of these cell line with respect to conventional drugs. In conclusion, 3D scaffolds could be an ideal platform for studying the mechanisms that regulate ACT growth and survival and also improving novel therapeutic approaches for treatment-resistant thyroid cancer.The functional role of fatty acid 2-hydroxylase (FA2H) is controversial in the field of cancer biology due to the dual role of FA2H, particularly related to its interaction with triple-negative breast cancer (TNBC). A previous biochemical- and clinical-focused study suggested that FA2H could dampen TNBC aggressiveness. However, another epidemiological study demonstrated that FA2H expression is associated with shorter disease-free survival in TNBC cases. We reported that FA2H is a peroxisome proliferator-activated receptor α (PPARα)-regulated gene in human breast cancer MDA-MB-231 cells, in vitro experimental models for TNBC analysis. PPARα activation by its ligand reportedly results in an aggressive MDA-MB-231 cell phenotype, as well as estrogen receptor α (ERα)-positive MCF-7 cells. The results of this study show that i) MDA-MB-231 cells express very low levels of FA2H compared to the MCF-7 cells, reflecting a low basal-level PPARα-driven transcriptional activity compared to the MCF-7 cells, and ii) the increased FA2H expression stimulates the MDA-MB-231 and MCF-7 breast cancer cell migration without affecting proliferation.