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1.
Article in Chinese | WPRIM | ID: wpr-802035

ABSTRACT

Objective:To investigate the intervention effect of panax notoginseng saponins (PNS) on epithelial-mesenchymal transition (EMT) of rat renal tubular epithelial cells (NRK-52E) induced by transforming growth factor-β1(TGF-β1), and analyze the mechanism based on the silent information regulation 2 homolog 1(SIRT1)/TGF-β1/Smad signaling pathway. Method:NRK-52E were cultured in DMEM medium with 10% fetal bovine serum, and divided into normal control group, TGF-β1 group (5 μg·L-1), resveratrol (RSV) group (50 mg·L-1), EX527 group (10 μmol·L-1), Panax notoginseng saponins (PNS) group (100 mg·L-1), and EX527+ PNS group (10 μmol·L-1+100 mg·L-1). Then cells were collected after drug intervention for 48 h. The expressions of α-SMA,E-cadherin,SIRT1,TGF-β1,Smad3,Smad4 mRNA in each group were detected by Real-time PCR. The protein expressions of α-SMA, E-cadherin,SIRT1 and TGF-β1 were detected by Western blot. Result:Compared with normal group, mRNA and protein expressions of α-SMA increased obviously(PPβ1 group. Compared with TGF-β1 group, mRNA and protein expressions of α-SMA decreased significantly(PPPβ1,Smad3,and Smad4 decreased(PConclusion:PNS can prevent the occurrence of EMT of renal tubular epithelial cells induced by TGF-β1, and the mechanism may be related to active SIRT1 to inhibit TGF-β1/Smad pathway.

2.
Article in Chinese | WPRIM | ID: wpr-487939

ABSTRACT

Objective To observe the neural protection of 3-n-butylphthalide (NBP) injection in focal cerebral ischemia-reperfusion rats. Methods 160 male Sprague-Dawley rats were randomly divided into sham group (n=10), ischemia-reperfusion group (IR group, n=50), high-dose NBP treatment group (high-dose group, n=50), middle-dose NBP treatment group (middle-dose group, n=25) and low-dose NBP treatment group (low-dose group, n=25). The later 4 groups were occluded the middle cerebral artery for 2 hours and reperfused. The sham group was sacrificed 24 hours after operation, and the other groups at 6, 12, 24, 48 and 72 hours after reperfusion, in which 5 of them were stained with TdT mediated dUTP Nick End Labeling (TUNEL) to observe the neuronal apoptosis, and immunohistochemistry to observe the expression of silent information regulation 2 homolog 1 (SIRT1) and peroxisome proliferator-activated receptorγcoactivator-1α(PGC-1α);the other 5 of sham group, IR group and high-dose group were observed with quantitative real-time PCR of SIRT1 and PGC-1α. Results Compared with the IR group, the number of apoptotic cells decreased and the SIRT1 and PGC-1αpositive cells increased in all NBP groups at each time (F>160.60, P4.13, P<0.01). Conclusion NBP can protect brain from apoptosis in focal cerebral ischemia-reperfusion rats, which may relate to more ex-pression of SIRT1 and PGC-1α.

3.
Chinese Journal of Epidemiology ; (12): 613-616, 2011.
Article in Chinese | WPRIM | ID: wpr-273129

ABSTRACT

Objective To explore the role of silent information regulation 2 homolog 1 (SIRTl) in the regulation of IL-lβ mRNA transcription in lipopolysaccharide(LPS) tolerant THP-1 cells. Methods THP-1 human promonocyte model of endotoxin tolerance that simulates the sepsis leukocyte phenotype was used. Chromatin immunoprecipitation assay (ChIP) and real-timePCR were applied to quantify the binding of SIRTl and histone H3 lys9/H4 lysl6 acetylation to IL-1β promoter. IL-1β mRNA transcription was studied after knocking down the SIRTl. Results Thebinding of SIRTl to IL-1β promoter increased about 5 times in tolerant THP-1 cells (P<0.05) , which was accompanied by the low level of histone H3 lys9/H4 lysl6 acetylation (P<0.05, compared with normal cells). Knocking-down of SIRTl increased the transcription of IL-1β mRNA up to the level of 68% of normal cells (P<0.05) ,which was accompanied by the increase of histone H3 lys9/H4 lysl6 acetylation (P<0.05). However,there was no significant difference of p65 lys310 acetylation between normal and tolerant cells. Conclusion SIRTl inhibited the IL-1 β mRNA transcription in tolerant THP-1 cells but had not related to p65 lys310 acetylation. However, it was related to IL-1 p promoter acetylation.

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