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1.
Basic & Clinical Medicine ; (12): 745-750, 2018.
Article in Chinese | WPRIM | ID: wpr-693978

ABSTRACT

Objective To explore the mechanism underlying a selective liver nitric oxide donor V-PYRRO/NO effects on the gene expression of LTC4 synthase(LTC4S) during hepatic ischemia reperfusion(I/R).Methods Adult male SD rats were divided into 3 groups:control group(sham),ischemic-reperfusion group(I/R) and V-PYRRO/NO group. Liver subjected to 1 hour of partial hepatic ischemia followed by 5 hours of reperfusion, saline or V-PYRRO/NO[1.06 mmol/(kg·h)] administered intravenously. The mRNA expression of LTC4S in rat liver was examined by RT-PCR method,the protein expressions of NF-κB p65,p50 and IκB in liver cell lysates and nu-clear extracts were detected by Western blot analysis. Results Hepatic mRNA expression of LTC4S in I/R group was higher than that in sham group(P<0.05), whereas it was lower in V-PYRRO/NO group than that in I/R group(P<0.05). Moreover,compared with sham group,the protein expressions of NF-κB p65 and p50 in nucleus extract were markedly increased(P<0.01) but significantly decreased in cytoplasm(P<0.01) in I/R group. V-PYRRO/NO reversed completely the increase of these protein expressions in nucleus extract (P<0.05) and the decrease of them in cytoplasm(P<0.01,P<0.05) during hepatic I/R injury.However,IκB protein in three groups did not change. Immunohistochemistry staining revealed that no marked positive staining for NF-κB p65 was found in sham liver,I/R liver exhibited strong cytoplasmic and nuclear positive staining for NF-κB p65,but V-PYRRO/NO I/R group liver presented slight cytoplasmic and nuclear staining. Conclusions V-PYRRO/NO may down-regulate LTC4S mRNA expression by inhibiting NF-κB activation independent of IκB during hepatic I/R injury.

2.
JCPSP-Journal of the College of Physicians and Surgeons Pakistan. 2014; 24 (5): 373-374
in English | IMEMR | ID: emr-142370
3.
Chinese Journal of Dermatology ; (12)2003.
Article in Chinese | WPRIM | ID: wpr-674250

ABSTRACT

Objective To investigate the possible mechanism of curcumin inhibition to murine melanoma growth.Methods Melanoma cell line B16F10 was injected subcutaneously into the outer side of mouse right thigh to establish a melanoma-bearing mouse model.Seven days after the establishing the model, these mice were treated with intraperitoneal injection of curcumin at 50 and 100 mg/kg respectively or RPMI 1640 culture medium as control.Fourteen days later,the mice were killed,tumor weight was calculated;the tumor nuclear factor?B activity and survivin mRNA expression were measured by Western blot and RT-PCR,respectively.Results The tumor weight was significantly lower in the curcumin-treated mice than that in the controls (P

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