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1.
Article in Chinese | WPRIM | ID: wpr-880776

ABSTRACT

OBJECTIVE@#To investigate the protective effect of arctiin with anti-inflammatory bioactivity against triptolide-induced nephrotoxicity in rats and explore the underlying mechanism.@*METHODS@#Forty SD rats were divided into 4 groups for gastric lavage of normal saline, arctiin (500 mg/kg), triptolide (500 μg/kg), or both arctiin (500 mg/kg) and triptolide (500 μg/kg). Blood samples were collected for analysis of biochemical renal parameters, and the renal tissues were harvested for determining the kidney index and for pathological evaluation with HE staining. In the @*RESULTS@#In SD rats, arctiin significantly antagonized triptolide-induced elevation of BUN, Scr and kidney index (@*CONCLUSIONS@#Arctiin can protect the kidney from triptolide-induced damages in rats possibly through the anti-inflammatory pathway.


Subject(s)
Animals , Anti-Inflammatory Agents , Diterpenes/toxicity , Epoxy Compounds/toxicity , Furans , Glucosides , Kidney/drug effects , Phenanthrenes/toxicity , Rats , Rats, Sprague-Dawley
2.
Article in Chinese | WPRIM | ID: wpr-355300

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the molecular?mechanisms by which triptolide induces apoptosis of human acute T lymphocytic leukemia Jurkat cells.</p><p><b>METHODS</b>MTT assay was employed to detect the proliferation inhibition of Jurkat cells by triptolide, and the IC50 was calculated by OriginPro8. Flow cytometry was used to analyze apoptosis of Jurkat cells. Np9 mRNA levels were detected by RT-PCR and analyzed quantitatively by Kodak 1D 3.6 software. Correlation between the inhibition of Np9 transcription and the cell apoptosis was analyzed by SPSS 19.0.Western blotting was employed to determine Np9 downstream signaling molecules c-myc, β-catenin, ERK, AKT and Notch1 protein level in Jurkat cells after exposure to different concentrations of triptolide for 48 h.</p><p><b>RESULTS</b>Triptolide treatment resulted in dose-dependent inhibition of Jurkat cells proliferation and its IC50 was 12.7 nmol/L. Triptolide induced apoptosis of Jurkat cells in dose- dependent manner. Furthermore, triptolide inhibited Np9 mRNA transcription level in Jurakt cells in a dose-dependent manner. There was a correlation between the triptolide-mediated the apoptosis and the inhibition of Np9 transcription of Jurkat cells (R(2)=0.907). Western blotting results displayed that triptolide inhibited transcription levels of Np9 mRNA with a concomitant decrease of its downstream signaling molecules c-myc, β-catenin, ERK, AKT and Notch1 at protein levels.</p><p><b>CONCLUSION</b>Inhibition of HERV-K Np9 mRNA and its downstream signaling molecules c-myc, β-catenin, ERK, Akt and Notch1 protein might be one of important molecular?mechanisms by which triptolide induces apoptosis of human acute T lymphocytic leukemia Jurkat cells.</p>


Subject(s)
Apoptosis , Diterpenes , Pharmacology , Endogenous Retroviruses , Genetics , Epoxy Compounds , Pharmacology , Flow Cytometry , Gene Products, env , Genetics , Humans , Jurkat Cells , Phenanthrenes , Pharmacology , Precursor T-Cell Lymphoblastic Leukemia-Lymphoma , Pathology , Transcription, Genetic
3.
Article in Chinese | WPRIM | ID: wpr-441806

ABSTRACT

Objective To investigate the role of recombinant Vibrio vulnificus cytolysin (rVvhA) in inducing THP-1 cells damage and study the pathway of associated calcium influx .Methods Inverted mi-croscope, CCK-8 cell proliferation kit, Fluo3/AM staining and caspase activity detection were performed to analyze the damage of THP-1 cells induced by rVvhA and the pathway of calcium influx .Results rVvhA had cytotoxic effects on THP-1 cells in a dose-dependent manner .The concentrations of extracellular K +and LDH were respectively up-regulated after 1 h and 6 h of 12 μg/ml rVvhA intervention .Verapamil , Mibe-fradil and SKF-96365 could not prevent the influx of free Ca 2+induced by rVvhA .The activities of caspase-3 and caspase-9 were singanificantly enhanced by rVvhA in a time-dependant manner .Conclusion rVvhA can induce THP-1 cells damage through triggering extracellular calcium influx via porous channel on cell membrane.Moreover, rVvhA might induce THP-1 cell apoptosis through activating caspase-9/3-dependent pathway .

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