OBJECTIVETo explore the effect of Yinqiao detoxifcation oral liquid on activity of natural killer cells (NK) and serum content of TNF-alpha, TGF-beta1 of BALB/C nude mouse infected by influenza virus.

METHODTo establish infected mice model by FM1 followed by intragastric administration of Yinqiao detoxifcation oral liquid for treatment. LDH method was used to observe NK cells. ELISA method was used to determine the levels of TNF-alpha, TGF-beta1, in serum on 1st, 3rd, 5th, 7th days after infection.

RESULTComparing to the normal group, the NK activity of the model group was significantly increased on 1 dpi (day post infection), and significantly decreased on 3, 5, 7 dpi. The NK activity of three dosage groups (5, 10, 20 g x kg(-1)) of Yinqiao detoxifcation oral liquid were respectively higher than that of the model on 3, 5, 7 dpi, especially with high dose (P < 0.01). The serum level of TNF-alpha and TGF-beta1 of model group is higher than that of normal group on 1, 3, 5, 7 d. Compared with model group, the serum level of Yinqiao detoxifcation oral liquid groups (5, 10, 20 g x kg(-1)) were decreased in different degree on every time point, especially the serum level of the higher dose of Yinqiao detoxifcation oral liquid decreased on 3 dpi (P < 0.05), Yinqiao detoxifcation oral liquid inhibit the serum level of TGF-beta1 in a dose-dependent manner.

CONCLUSIONYinqiao detoxifcation oral liquid could enhance the activity of NK cell and decrease the serum level of TNF-alpha and TGF-beta1 of the mice infected by influenza virus.

Administration, Oral ; Animals ; Disease Models, Animal ; Drugs, Chinese Herbal ; administration & dosage ; Humans ; Influenza A virus ; immunology ; physiology ; Influenza, Human ; drug therapy ; immunology ; virology ; Killer Cells, Natural ; drug effects ; immunology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Random Allocation ; Transforming Growth Factor beta1 ; immunology ; Tumor Necrosis Factor-alpha ; immunology

Objective To evaluate the effectiveness of a rat model for comorbidity of Tourette syndrome and anxiety with empty water bottle stimulation plus iminoodipropionitrile(IDPN) injection.Methods The 48 male SD rats were randomly divided into four groups:the blank control group,the TS group,the anxiety group and the comorbidity group.The blank control group was injected with saline for 7 days.The TS groop was injected with 3,3-iminodipropionitrile (IDPN) with 250 mg/kg once a day for 7 consecutive days.The anxiety group was given empty water bottle stimulation for 21 consecutive days.The comorbidity group was given empty water bottle stimulation plus IDPN injection.At the end of the 3rd week,the behavioral changes of the stereotyped movement,elevated plus-maze and open field of the rats in each group were measured,and the contents of monoamine neurotransmitters in striatum and hippocampus were determined by HPLC.Results The results of stereotyped movement showed that there was no significant difference between the groups except for the blank control group.The elevated plus-maze test showed that the 0E/TE values of the comorbidity group (21.33±11.35) ％ and the anxiety group (17.68±16.89) ％ were significantly decreased,lower than that of the blank control group (73.24± 19.33) ％ and TS group(61.43±21.84) ％.The results of open field test showed that the total scores of open field in the comorbidity group(15.22±9.87)and anxiety group (11.17±10.76) were lower than that of the blank control group (41.86±33.30) and TS group(48.83± 17.65) (P＜0.01).However,there was no significant difference between the comorbidity group and the anxiety group.The test of monoamine neurotransmitters in striatum showed that the content of HIAA in the comorbidity group(0.03±0.00) ng/mg was the highest,and that of the TS group and anxiety group (0.02±0.00) ng/mg was higher than that of the blank control group (0.01±0.00) ng/mg (P＜0.01).The DA test showed that the content of DA in the comorbidity group (0.03±0.00) ng/mg was the highest,and that of the comorbidity group,TS group(0.02±0.00) ng/mg and anxiety group was higher than that of the blank control group(0.01±0.00) ng/mg (P＜0.01).The expression of 5-HT was most significant among the groups (P＜0.01),and there was significant difference between the anxiety group ((0.011 ± 0.001) ng/mg)and the comorbidity group ((0.014±0.002) ng/mg) (P＜0.01).The expression of HVA in the three model groups ((0.05±0.00) ng/mg) was higher than that in the blank group ((0.02±0.00) ng/mg) (P＜ 0.01).The expression of DOPAC in the TS group ((0.23±0.02) ng/mg) was higher than that in the blank control group((0.16±0.01) ng/mg) and comorbidity group ((0.16±0.02) ng/mg) (P＜0.01).The test of monoamine neurotransmitters in hippocampus showed that the content of 5-HT in the comorbidity group ((0.14±0.02) ng/mg) was the highest,followed by the anxiety group ((0.1 ± 0.03) ng/mg) and the TS group ((0.07±0.04) ng/mg),which were all higher than the blank control group((0.04±0.03) ng/mg) (P＜0.05,P＜0.01),and there were significant differences between the comorbidity group and the TS group or anxiety group (P＜0.01).The expressions of HIAA and HVA were higher in the comorbidity group((0.44±0.04)ng/mg,(0.01±0.00) ng/mg),TS group ((0.46±0.15) ng/mg,(0.01 ±0.01) ng/mg) and anxiety group ((0.46±0.08)ng/mg,(0.01±0.00) ng/mg) than that in the blank control group((0.21±0.10)ng/mg,(0±0) ng/mg) (P＜0.05,P＜0.01).Conclusion This study confirms the reliability of the model and it is an ideal animal model for the study of TS with comorbidity of anxiety,which can be used for follow-up research.

OBJECTIVE：To in vestigate the effects of dexmedetomidine （Dex）on SIRT 1/Akt/GSK3β/β-catenin signaling pathway in cerebral injury of sepsis model rats ，and explore the mechanism of its protecitve effect on cerebral injury. METHODS ： A total of 80 male SD rats were randomly divided into sham operation group （Sham group ），sepsis group （CLP group ），CLP+Dex group（10 μg/kg Dex），CLP+Dex+Sirtinol group （10 μg/kg Dex+2 μL/100 g SIRT 1 inhibitor sirtinol ），with 20 mice in each group. Two hours before modeling ，CLP+Dex+Sirtinol group was injected with sirtinol via lateral ventricle. Sepsis model was induced by cecal ligation and perforation in each group （in sham group ，only operation was performed but no ligation was performed）. At 0，3，6 h after modeling ，CLP+Dex group and CLP+Dex+Sirtinol group were given Dex （10 μg/kg） intraperitoneally，Sham group and CLP group were given constant volume of normal saline intraperitoneally. Cerebral tissue water content，Evans blue （EB）content，apoptosis in cerebral cortex ，the levels of IL- 1β and TNF-α in cerebral tissue as well as the protein expression of SIRT 1，p-Akt，p-GSK3β and β-catenin in hippocampus were detected 24 h after last medication. RESULTS ： Compared with Sham group ，cerebral tissue water content ，EB content ，the number of apoptotic cells in cerebral cortex as well as the levels of IL- 1β and TNF-α in cerebral tissue were increased significantly（P＜0.05），while the protein expression of SIRT 1， p-Akt，p-GSK3β and β-catenin in hippocampus were decreased significantly （P＜0.05）. Compared with CLP group ，cerebral tissue water content ，EB content ，the number of apoptotic cells in cerebral cortex as well as the levels of IL- 1β and TNF-α in cerebral tissue were decreased significantly in CLP+Dex group （P＜0.05），while the protein expression of SIRT 1，p-Akt，p-GSK3β and β-catenin in hippocampus were increased significantly （P＜0.05）. Sirtinol could significantly reverse the above-mentioned cerebral protection and factor regulation effects of Dex （P＜0.05）. CONCLUSIONS ：Dex can protect the cerebral tissue of sepsis model rats，which may play an anti-inflammatory and anti-apoptotic role by activating SIRT 1/Akt/GSK3β/β-catenin signaling pathway ，so as to reduce cerebral edema ，protect blood-brain barrier and reduce cerebral injury.