Objective: To establish an ischemia-reperfusion injury model of rat cerebral microvascular endothelial cells (MVECs) in vitro, and to explore the relationship between nuclear factor-kappa B (NF-kappaB) and the protective effects of Qingkailing effective components (hyocholic acid, taurocholic acid, baicalin, jasminoidin, Pinctada martensii) on MVECs.
Methods: Brain MVECs of male rats were digested with trypsin and subcultured, then the content of MVECs was adjusted to 1x10 (5)/mL and the MVECs were divided into normal control group, untreated group, hyocholic acid group, taurocholic acid group, baicalin group, jasminoidin group, Pinctada martensii group and nimodipine group, with six holes in each group. Except for the normal control group, the MVECs in the other groups were exposed in oxygen and glucose deprivation (OGD) circumstance in vitro to simulate ischemia-reperfusion injury. Immunocytochemical staining and image analysis system were used to observe the expression of NF-kappaB protein.
Results: Under a light microscope, the nuclei of MVECs in the normal control group were blank. Staining intensity of NF-kappaB protein in the nucleus in the untreated group was much deeper than that in the endochylema, with NF-kappaB shifted to nucleus after activation; a small quantity of NF-kappaB protein were expressed in the border of nucleus next to endochylema in groups of Qingkailing effective components, and the NF-kappaB protein expression was weaker than that in the untreated group. With the image analysis, we found that transmittance of nucleus and endochylema in the untreated group was significantly lower than that in the normal control group (P<0.01). Transmittance of nucleus and endochylema in the treated groups was higher than that in the untreated group (P<0.05, P<0.01).
Conclusion: Qingkailing effective components have significant effect in inhibiting NF-kappaB protein transferring from endochylema to nucleus in vitro.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.3736/jcim20090208 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Measurement of CP Violation Observables in D^{+}→K^{-}K^{+}π^{+} Decays.
Phys Rev Lett
December 2024
Institute of Physics, Ecole Polytechnique Fédérale de Lausanne (EPFL), Lausanne, Switzerland.
A search for violation of the charge-parity (CP) symmetry in the D^{+}→K^{-}K^{+}π^{+} decay is presented, with proton-proton collision data corresponding to an integrated luminosity of 5.4 fb^{-1}, collected at a center-of-mass energy of 13 TeV with the LHCb detector. A novel model-independent technique is used to compare the D^{+} and D^{-} phase-space distributions, with instrumental asymmetries subtracted using the D_{s}^{+}→K^{-}K^{+}π^{+} decay as a control channel.
View Article and Find Full Text PDFcSTAR analysis identifies endothelial cell cycle as a key regulator of flow-dependent artery remodeling.
Sci Adv
January 2025
Yale Cardiovascular Research Center, Yale School of Medicine, New Haven, CT 06511, USA.
Fluid shear stress (FSS) from blood flow sensed by vascular endothelial cells (ECs) determines vessel behavior, but regulatory mechanisms are only partially understood. We used cell state transition assessment and regulation (cSTAR), a powerful computational method, to elucidate EC transcriptomic states under low shear stress (LSS), physiological shear stress (PSS), high shear stress (HSS), and oscillatory shear stress (OSS) that induce vessel inward remodeling, stabilization, outward remodeling, or disease susceptibility, respectively. Combined with a publicly available database on EC transcriptomic responses to drug treatments, this approach inferred a regulatory network controlling EC states and made several notable predictions.
View Article and Find Full Text PDFTau phosphorylation suppresses oxidative stress-induced mitophagy via FKBP8 receptor modulation.
PLoS One
January 2025
Department of Anesthesiology & Perioperative Medicine, University of Rochester, Rochester, New York, United States of America.
Neurodegenerative diseases are often characterized by mitochondrial dysfunction. In Alzheimer's disease, abnormal tau phosphorylation disrupts mitophagy, a quality control process through which damaged organelles are selectively removed from the mitochondrial network. The precise mechanism through which this occurs remains unclear.
View Article and Find Full Text PDFSingle cell RNA-seq reveals that granulosa cells are a target of phthalate toxicity in the ovary.
Toxicol Sci
January 2025
Department of Chemistry and Environmental Science, New Jersey Institute of Technology, Newark, NJ, 07103.
Phthalates are known endocrine disrupting chemicals and ovarian toxicants that are used widely in consumer products. Phthalates have been shown to exert ovarian toxicity on multiple endpoints, altering transcription of genes responsible for normal ovarian function. However, the molecular mechanisms by which phthalates act on the ovary are not well understood.
View Article and Find Full Text PDFSingle-nucleus and spatial landscape of the sub-ventricular zone in human glioblastoma.
Cell Rep
January 2025
The Brain Tumor Translational Laboratory, Department of Cell Biology and Physiology, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA; University of New Mexico Comprehensive Cancer Center, Albuquerque, NM 87131, USA. Electronic address:
The sub-ventricular zone (SVZ) is the most well-characterized neurogenic area in the mammalian brain. We previously showed that in 65% of patients with glioblastoma (GBM), the SVZ is a reservoir of cancer stem-like cells that contribute to treatment resistance and the emergence of recurrence. Here, we build a single-nucleus RNA-sequencing-based microenvironment landscape of the tumor mass and the SVZ of 15 patients and two histologically normal SVZ samples as controls.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!