Wenxia Changfu Formula () induces apoptosis of lung adenocarcinoma in a transplanted tumor model of drug-resistance nude mice / 中国结合医学杂志

<p><b>OBJECTIVE</b>To explore the apoptosis mechanism of Wenxia Changfu Formula (, WCF) in reversing drug resistance of lung cancer in vivo.</p><p><b>METHODS</b>Thirty model mice were randomly assigned to three groups: control group, cisplatin (CDDP) group, and WCF group. A transplanted tumor model of lung adenocarcinoma was established in all groups. Mice in the WCF group received intragastric administration of WCF (0.2 mL/10 g body weight) everyday in addition to CDDP intraperitoneally (5 mg/kg body weight) twice a week. The mice in the CDDP group received CDDP intraperitoneally (5 mg/kg body weight) twice a week, while the control group received normal saline intraperitoneally (0.2 mL/10 g body weight) everyday. The weight of the nude mice and respective tumors, tumor volume and tumor-inhibiting rate were measured. Electron microscopy was used to observe the existence of apoptosis body. Apoptosis index (AI) was detected by TdT-mediated dUTP nick end labeling staining. The expression of Fas and FasL mRNA was investigated by reverse transcription polymerase chain reaction, while immunohistochemistry was applied to detect the protein expression of Fas and FasL, caspase-3 and caspase-activated DNase (CAD), respectively.</p><p><b>RESULTS</b>Compared with CDDP group and control group, WCF could significantly reduce the tumor volume from the 19th day and alleviate the tumor weight (P <0.05), and the apoptosis body was found in tumor cells in the WCF group. WCF could also enhance the level of AI, up-regulate the expression of caspase apoptosis pathway related protein caspase-3 and CAD, as well as the expression of Fas, FasL mRNA and protein (P <0.05).</p><p><b>CONCLUSION</b>WCF could improve the sensitivity of tumor cells to CDDP and reverse the drug resistance by inducing the apoptosis.</p>

Experimental studies on treatment of depression with YJ-XCC1Z3 in mouse models / 中国中药杂志

<p><b>OBJECTIVE</b>To evaluate the pre-clinical effect of YJ-XCC1Z3 on the treatment of depression with the mice mouse.</p><p><b>METHOD</b>YJ-XCC1Z3 was administered at the dose of 405 mg x kg(-1) and 135 mg x kg(-1) to observe the locomotor activity with the mouse locomotor activity recorder apparatus, to observe the effect of YJ-XCC1Z3 on the duration of immohility in the mouse forced swimming test and tail suspension test, to observe the effect of YJ-XCC1Z3 on the body temperature and the metabolism of monoamine neurotransmitters in mouse brain in the mouse model of reserpine induced hypothermia, and to observe the effect of YJ-XCC1 Z3 on the times of 5-HTP induced head-twitches in mice.</p><p><b>RESULT</b>There were no significant changes in the locomotor activity, but a significant reduction in the immobility time was observed in the mice treated with YJ-XCC1Z3 405 mg x kg(-1) and imipramine in the forced swimming test and the tail suspension test. YJ-XCC1Z3 135 mg x kg(-1) and 405 mg x kg(-1) could improve the range of reserpine induced hypothermia in mice, and the latter could also enhance the times of 5-HTP induced head-twitches in mice. YJ-XCC1Z3 405 mg x kg(-1) and 135 mg x kg(-1) could increase the content of 5-HT and NE and decrease the ratio of 5-HIAA/5-HT in mouse brain, but the dose of 405 mg x kg(-1) could decrease the content of DA. The dose of 405 mg x kg(-1) could increase the content of 5-HIAA and had no obvious effect on the content of HVA and DOPAC.</p><p><b>CONCLUSION</b>YJ-XCC1Z3 shows potent antidepressant effect by improving the behaviour of the mouse in depression and not inducing hyperlocomotion in the mice. This effect results in the increase of the content of 5-HT and NE in the mouse brain. YJ-XCC1Z3 can decrease the metabolism of 5-HT to effect the content of 5-HT.</p>