1.Effect of remifentanil combined with dezocine or fentanyl on analgesia in cholecystectomy
Xingui XIA ; Haiyan DING ; Shizhong YANG
Chinese Journal of Biochemical Pharmaceutics 2016;36(6):106-108
Objective To investigate the effect of remifentanil combined with dezocine or fentanyl on analgesia in patients with cholecystectomy. Methods A total of 98 patients with cholecystectomy from our hospital were collected, patients were randomly divided into the experimental group and control group with 49 cases in each group.Patients in the control group were treated by remifentanyl combined with fentanyl intravenous injection and patients in the experimental group were treated by remifentanyl combined with dezocine intravenous injection.The analgesia and sedation score and vital signs changes at recovery time (T1), after recovery 1h (T2), 2 h (T3), and the revival time, extubation time and adverse reactions were compared between two groups.Results The visual analogue scale score in experimental group at T1 , T2 , T3 and Ramsay sedation scale ( RSS) at T2 , T3 were lower than control group, the revival time and extubation time in experimental group were lower than control group, with significant difference (P<0.05). There was no significant difference at T0 ,T1 ,T2 and T3 between two groups.There was no respiratory depression happened in two groups, and there was no significant difference in adverse drug reaction between control group and experimental group (16.33% vs.10.20%).Conclusion The remifentanil combined with dezocine has a good inhibitory effect on postoperative hyperpathia with less adverse reactions.
3.Role of SphK1 in renal tubulointerstitial fibrosis and its mechanism
Chunyang DU ; Xia XIAO ; Xingui WANG ; Jiao FU ; Yiping FENG ; Fengli HU ; Enli CHEN ; Yunzhuo REN
Chinese Pharmacological Bulletin 2017;33(2):212-217,218
Aim To investigate the effect of sphingo-sine kinase 1 (SphK1 )on unilateral ureteral obstruc-tion(UUO)-induced tubulointerstitial fibrosis and ex-plore the possible mechanism.Methods The CD-1 mice were randomly divided into four groups:sham-op-eration group(Sham),PF-543 treatment control group (Sham +PF-543),model group(UUO)and PF-543 treatment group(UUO +PF-543).On 1 ,3,7 and 1 4 d after operation,eight mice were selected randomly from each group and sacrificed.The protein expressions of SphK1 ,mature TGF-β1 ,FN,ColⅠ,LC3,Beclin1 ,Atg5 and Atg1 2 were observed by Western blot.The histo-logical changes were examined by Masson′s trichrome stain.Immunhistochemistry was performed to measure the levels of expression of SphK1 ,FN and Col Ⅰ. Transmission electron microscope was used to observe the autophagic body.Results SphK1 expression and autophagy were both upregulated in a mouse model of kidney fibrosis induced by UUO. Meanwhile, in-creased mature TGF-β1 and deposition of extracellular matrix(ECM)were observed in tubulointerstitial areas compared with sham-operated mice.After intraperito-neal injection with the SphK1 specific inhibitor PF-543 in UUO mice,enhanced expression of SphK1 and acti-vated autophagy were significantly abrogated.Howev-er,aggravation of renal fibrosis was detected when SphK1 inhibitor PF-543 was applied to suppress SphK1 expression in UUO mice.Conclusion SphK1 activa-tion is renoprotective through the induction of autoph-agy in the pathogenesis of kidney fibrosis.