ABSTRACT
[ ABSTRACT] AIM:To observe the effect of ginsenoside Rb 1 on the proliferation and the expression of serotonin transporter (SERT), 5-hydroxytryptamine 1B receptor (5-HT1BR) in rat pulmonary artery smooth muscle cells (PASMCs) under hypoxia condition and the relationship with Rho /Rho-kinase signal pathway .METHODS: PASMCs were isolated from the adult male SD rats and primarily cultured .The subcultured cells from the 4th generation to the 6th generation were harvested and divided into normal group , and hypoxia group , different concentrations of Rb 1 incubation groups treated with 50, 100 and 200 mg/L ginsenoside Rb1 under hypoxia (HR50, HR100 and HR200 groups, respectively).The viability of the PASMCs was measured by CCK-8 assay.BrdU positive cells were determined using flow cytometry .The expression of serotonin transporter and 5-HT1BR at mRNA and protein levels was detected by RT-PCR and Western blot, respectively. The PASMCs were randomly divided into normal group , hypoxia group , HR200 group and hypoxia +Y-27632 incubation group ( HY group ) .The mRNA expression of Rho-kinase and phosphorylated myosin phosphatase target subunit 1 ( p-MYPT1) protein level were investigated by RT-PCR and Western blot, respectively.RESULTS: Compared with normal group, the proliferation of PASMCs in hypoxia group was significantly increased (P<0.01).The cell viability and the ex-pression of SERT and 5-HT1B R at mRNA and protein levels in all different concentrations of Rb 1 groups were obviously de-creased compared with hypoxia group ( P<0.05 ) .The mRNA expression of Rho-kinase and protein level of p-MYPT1 were markedly decreased in HR200 group, and no significant difference compared with HY group was observed ( P <0.01).CONCLUSION: Treatment with ginsenoside Rb1 might prevent hypoxia-induced proliferation of PASMCs and over-expression of SERT and 5-HT1B R through inhibiting the Rho/Rho-kinase pathway .
ABSTRACT
[ ABSTRACT] AIM:To explore the effect of dexmedetomidine ( DEX) on the CCAAT/enhancer-binding protein-homologous protein ( CHOP) pathway during lung ischemia-reperfusion ( I/R) in mice.METHODS:C57BL/6J male mice were randomly divided into sham operation group ( sham group) , lung ischemia/reperfusion group ( I/R group) , ischemia/reperfusion +normal saline group ( I/R+NS group ) and ischemia/reperfusion+dexmedetomidine group ( I/R+DEX group) .Dexmedetomidine was infused intraperitoneally with 25 μg/kg for 30 min prior to the ischemia period in I/R+DEX group, the normal saline was administrated with the same volume of dexmedetomidine in I/R+NS group.After fini-shed the 3 h-reperfusion period , the left lung tissues were harvested to determine lung wet/dry weight ( W/D) , the total lung water content ( TLW) , and index of quantitative evaluation for alveolar damage ( IQA) .Morphological observation and terminal-deoxynucleotidyl transferase mediated nick end labeling ( TUNEL) were applied to evaluate the structure changes and the apoptosis index (AI) of the lung tissues.The expression of CHOP and glucose-regulated protein 78 (GRP78) at mRNA and protein levels in the lung tissues was detected by Western blot and RT-PCR.RESULTS:Compared with sham group, the W/D, TLW, IQA, AI, the mRNA and protein expression of CHOP and GRP78 obviously increased, and the left lung tissues structure were damaged more obviously both in I/R group and I/R+NS group.Compared with I/R group, the W/D, TLW, IQA, AI and the protein and mRNA expression of CHOP in I/R+DEX group decreased, the injury of the left lung tissue structures induced by I/R in I/R+DEX group were also alleviated .CONCLUSION:DEX alleviates the lung I/R injury, which may be related to inhibition of apoptosis mediated by CHOP pathway.