Objective To study the effect of SYUIQ-5,a novel antitumor agent,on gene expression of hepatic cytochrome P450 in rats.Methods Male Sprague-Dawley rats were administered daily intraperitoneal dose of SYUIQ-5(0.1mg/kg,5mg/kg and 10mg/kg body weight) for 5 consecutive days.The levels of CYP 3A1,2B1/2,1A1,1A2 and 2E1 mRNA in rat liver were analyzed by reverse transcription-polymerase chain reaction(RT-PCR).Results The level of gene expression of CYP 1A1 was increased significantly compared with the control.The levels of CYP 3A1,2B1/2,1A2 and 2E1 mRNA were not changed by SYUIQ-5 treatment compared with the control.Conclusion A significant increase in the CYP 1A1 rather than CYP3A1,2B1/2,1A2 and 2E1 gene expression by SYUIQ-5 treatment is observed.

Aim To investigate the antidepressive-like effect of ethyl alcohol extract of Polyrhachis vicina Rog-er(EAPR),and its mechanism.Methods EAPR was prepared by ethanol extraction.Its anti-depressive effect was investigated by tail suspension test (TST) and forced swimming test (FST).Furthermore,repeated doses of reserpine was used for preparing the depres-sive rats.Results EAPR has definitely anti-depres-sive effect,as evidenced by the decreased immobility time in FST and TST at the doses of 8 and 4 g·kg -1 (P <0.05).In the repeated reserpine evoked depres-sive rats,EAPR antagonized the symptoms induced by monoamines depletion and attenuated the anhedonia, as manifested by reversed hypothermia,akinesia and sucrose consumption at the doses of 8 and 2 g·kg -1 (P <0.05,P <0.01).Neuro-chemical studies showed that AFPR significantly increased the concentration of monoamines,including 5-hydroxytryptamine (5-HT) and noradrenaline(NA)at the dose of 8 g·kg -1 (P <0.05),and had no effect on normal rats .Furthermore, EAPR increased the activity of superoxide dismutase (SOD)in serum,hippocampus and cerebral cortex at the dose of 8 g·kg -1 (P <0.05).Conclusion EA-PR possesses the definite antidep ressive properties, connected with the regulation of neurotransmitter me-tabolism and the nerve cells antioxidant effect.

Hepatotoxicity is a common side effect for patients treated with gefitinib, but the related pathogenesis is unclear and lacks effective predictor and management strategies. A multi-omics approach integrating pharmacometabolomics, pharmacokinetics and pharmacogenomics was employed in non-small cell lung cancer patients to identify the effective predictor for gefitinib-induced hepatotoxicity and explore optional therapy substitution. Here, we found that patients with rs4946935 AA, located in Forkhead Box O3 (FOXO3) which is a well-known autophagic regulator, had a higher risk of hepatotoxicity than those with the GA or GG variant (OR = 18.020, 95%CI = 2.473 to 459.1784, P = 0.018) in a gefitinib-concentration dependent pattern. Furthermore, functional experiments identified that rs4946935_A impaired the expression of FOXO3 by inhibiting the promotor activity, increasing the threshold of autophagy initiation and inhibiting the autophagic activity which contributed to gefitinib-induced liver injury. In contrast, erlotinib-induced liver injury was independent on the variant and expression levels of FOXO3. This study reveals that FOXO3 mutation, leading to autophagic imbalance, plays important role in gefitinib-induced hepatotoxicity, especially for patients with high concentration of gefitinib. In conclusion, FOXO3 mutation is an effective predictor and erlotinib might be an appropriately and well-tolerated treatment option for patients carrying rs4946935 AA.