This paper systematically summarizes treatment contraindicationsof the prescription Guizhi decotion, Mahuang decotion, Guizhi 2 yuebi 1 decotion, Daqinglongdecotion, Lingguizhugandecotion, Zhizichi decotion, Baihu decotion, Chengqi decoction, Zhuling decotion , Xiaochaihu decotion, Taohechengqi decotion, Guizhi adding Shaoyao decotion, Guizhi adding dahuang decotion, Sinidecotion, Huangqin decotion in Treatise on Febrile Disease. Doctors should pay attention to thesetreatment contraindications forbetter syndrome differentiational treatment, thus to improve its clinical efficacy.

Objective To investigate the effects of Mahuang-Xixin-Fuzi decoction on the plasma levels of interlcukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in allergic rhinitis in rats. Methods Thirty-two Wistar rats were randomly divided into a control group, a model group, a chlorpheniramine group, and a Mahuang-Xixin-Fuzi decoction group, with 8 rats in each group. Allergic rhinitis was induced by ovalbumin sensitization. Rats in the chlorpheniramine and Mahuang-Xixin-Fuzi decoction groups received intragastric administration of 0.01%chlorpheniramine and Mahuang-Xixin-Fuzi decoction 0.4 g (twice daily for 21 days), respectively. The plasma levels of IL-6 and TNF-αwere measured with enzyme-linked immunosorbent assay. Results The frequencies of sneezing (2.4 ± 0.9/30 min vs.18.5 ± 3.6/30 min) and nasal rubbing (4.2 ± 1.5/30 min vs. 31.2 ± 3.7/30 min) in the Mahuang-Xixin-Fuzi decoction group were significantly lower than those in the model group (all P<0.05). The plasma levels of IL-6 (153.00 ± 13.87 pg/ml vs. 230.38 ± 33.92 pg/ml) and TNF-α(21.25 ± 4.62 pg/ml vs. 56.38 ± 7.93 pg/ml) in the Mahuang-Xixin-Fuzi decoction group were significantly lower than those in the model group (all P<0.05). Conclusions Mahuang-Xixin-Fuzi decoction can reduce the plasma levels of IL-6 and TNF-α, and alleviate symptoms in allergic rhinitis in rats.

Archen,a kind of Anthraquinone,is one of active ingredients of Chinese herb Rhubarb.The researches showed that archen has ideal therapeutic effects on diseases of circulatory system,digestive system，nervous system and tumor. The paper reviewed related researches on pharmacology of archen from year 2004 to 2008 and made a summary of the researching development of it.

0.05).Except that the wet weight of the epididymis in high-dose group of apigenin was significantly different compared with middle-dose group of apigenin(P 0.05).Cell cycle analysis showed that compared with the negative control group,the percent of diploid cells in low and high-dose group was decreased,the proportion of G0/G1 phase cells in low-dose group of apigenin was reduced(P

Objective To explore the effects of clarithromycin on the expressions of histone deacetylase-2 (HDAC2) and glucocorticoid receptor (GR) of cigarette smoke-exposed asthmatic mice.Methods BALB/c mice were chosen to be the subjects of this study.They were raised to establish asthma model (OVA group);and mice in one asthma group were exposed to smoke (SEA group), one asthma group were treated with clarithromycin (CAM group) after smoke exposure.Control group mice were used as parallel comparison.The histopathological changes were studied to assess lung tissue inflammation.Cell counts in bronchoalveolar lavage fluid were also tested for airway inflammation.Histone deacelytase2 (HDAC2) activity of lung tissues was measured by qRT-PCR.HDAC2 and GR expressions in the lung tissue were detected by Western blot.Results Histopathologic observation showed massive infiltration of inflammatory cells in both OVA group and SEA group, while inflammation infiltration attenuated in CAM group.Compared with those in CAM group, the levels of IL-4 and IL-8 in bronchoalveolar lavage fluid of SEA group increased significantly (104.36±14.39 vs.65.49±10.82, 681.35±66.18 vs.321.49±90.37;P=0.031, 0.017).The expression of HDAC2 mRNA in CAM group was significantly higher than that in SEA group (0.062±0.013 vs.0.031±0.015, P=0.032).The expressions of HDAC2 protein (0.23±0.017 vs.0.49±0.022, P=0.033) and GR protein (0.19±0.014 vs.0.64±0.023, P=0.011) were significantly lower in SEA group than in CAM group.Conclusion Clarithromycin could attenuate airway inflammation in smoke-exposed asthmatic mice.The mechanism of action may be related to the expression of HDAC2 gene in the lower reaches by combining with GR.

Objective To observe The liver lipogenic gene expression of animal model of phlegm and dampness syndrome. Methods According to the theory "Obese people have much more phlegm and dampness", the animal model of phlegm and dampness was built by high fat feeding. After 10 weeks' high fat feeding, we examined liver HE slice, the level of lipids in the normal and model group rats .The liver lipogenic gene expression including LXRα, SREBP-1c, and FAS were detected by fluorescence real time quantative PCR. Results Compared with that of the normal group rat, there was increasing lipids both in serum and liver in the model rats. There was typical appearance of fatty accumulation in the liver cells examined by liver HE staining. The expression of SREBP-Ic and FAS was much higher in phlegm and dampness group than that in the normal group, although there was no difference in the expression of LXRα. Conclusion The fatty accumulation of liver cell in phlegm and dampness group has a close relation to the enhancement of the liver lipoganic gene expression.

Objective To investigate the relationship between single nucleotide polymorphisms (SNPs) of UGT1 A6 and aspirin response in a cohort of Chinese Han population.Methods A total of 323 ischemic stroke patients consecutively registered in Nanjing Stroke Registry Program from September 2011 to October 2014 were enrolled.Three SNPs (rs6759892,rs2070959 and rs1105879) of UGT1A6 were genotyped in these ischemic stroke patients.Association of genotypes and aspirin response was evaluated by generalized linear model.Indicated with the inhibition rate of platelets,aspirin response was assessed by thromboelastograph.Results The mutation allele (G) of rs2070959 was positively related to platelets inhibition (β =0.084,P =0.010,Pcorrected =0.029),especially in male (β =0.098,P =0.006,Pcorrected =O.019).The dominant models of rs6759892,rs1105879 were also modestly related to aspirin response (P=0.015,Pcorrected=0.046 in both SNPs) in male.Thus the polymorphisms of UGT1A6 showed a relationship with aspirin response,especially in males.Conclusions The results indicated that genetic polymorphism of UGT1A6 might have an effect on individuals' aspirin response,especially in males.These findings can help clinicians to optimize the antiplatelet therapy for ischemic stroke patients.

Stroke has become the leading cause of death in Chinese residents. As the cornerstone of the primary and secondary prevention of ischemic stroke, aspirin can prevent the occurrence and recurrence of ischemic stroke in a certain extent. However, some patients stil have vascular events after taking aspirin regularly or higher platelet aggregation rate. This phenomenon is caled aspirin resistance or aspirin low reactivity. This article reviews the occurrence, detection methods, and treatment measures of aspirin resistance in patients with ischemic stroke.

ObjectiveTo investigate the biological significance and mechanism of VEGF-C in esophageal tumor development,and correlation of CNTN-1 level with VEGF-C.MethodsThe expression of VEGF-C and its receptors in esophageal squamous cancer cell (ESCC) and in corresponding noncancerous esophageal tissue specimens were detected by real-tithe PCR.Esophageal squamous cancer cell line TE-1 was transinfected by VEGF-C overexpression and gene silencing vectors,respectively,and the relative amount of C/EBP bound to CNTN-1 promoter was determined by quantitative ChIP,to explore the possibility that VEGF-C was involved in development of esophageal cancer through mediating transcription of CNTN-1.ResultsThe mRNA levels of VEGF-C was significantly higher in ESCC than in normal esophageal tissues.VEGF-C expression was significantly increased in VEGF-C-overexpressing TE-1 cells compared to untransfected cells (mock).Cells transfected with either of the VEGF-C targeting shRNA vectors,shRNA-1 and shRNA-2,showed reduced VEGF-C transcripts (P ＜ 0.01 ).Expression levels of VEGF-C and CNTN-1 mRNA correlated significantly with each other.The binding site of C/EBP in CNTN-1 was detected by ChIP,and the relative amount of C/EBP binding to CNTN-1 promoter was significantly increased in TE-1 after transfecting by VEGF-C overexpression vector ( P ＜ 0.05).ConclusionVEGF-C and its receptor are highly expressed in esophageal cancer tissues,which may be associated with ESCC carcinogenesis and development.VEGF-C may influence on growth and migration in TE-1 cells through CNTN-1.

Objective To investigate the role of poly(ADP-ribose) polymerase (PARP) inhibitor PJ34 in regulating blood-brain barrier (BBB) permeability and matrix metalloproteinases-9 (MMP-9) expression in a mouse model of traumatic brain injury (TBI).Methods A total of 136 adult male BALB/c mice were randomly divided into sham-operated group,injured group and PJ34-treated group according to the random number table.Controlled cortical impact in mice was established.At 6 and 24hours postinjury,neurological deficit was evaluated,including motor,sensory,reflex and beam balance tests ; BBB permeability and brain water content were detected using Evans blue test and gravimetric technique; brain contusion volume was measured using HE staining; levels of MMP-9 in cytosolic fractions were detected using Western blotting.Results At 6 and 24 hours postinjury,neurological severity score in PJ34-treated group (8.00 ± 0.26,7.50 ±0.25) were lower than those in injured group (12.50 ±0.39,11.80 ± 0.32) ; brain contusion volume in PJ34-treated group [(11.25 ± 0.91) mm3,(13.55 ±1.06) mm3] was lower than those in injured group [(25.37 ± 1.75) mm3,(28.24 ± 1.51) mm3] ; BBB permeability in PJ34-treated group [(440.08 ± 3.10) μg/mg,(860.46 ± 3.86) μg/mg] was lower than those in injured group [(936.96 ± 4.71) μg/mg,(1 302.23 ± 5.89) μg/mg] (all P ＜ 0.01).Brain water content lowered significantly in PJ34-treated group than in injured group at 6 hours postinjury [(80.77 ± 0.76) ％ vs (82.55 ± 0.73) ％,P ＜ 0.0l],but between-group difference was not significant at 24 hours postinjury.Lower levels in MMP-9 were also observed in PJ34-treated group compared with injured group at 6 and 24 hours postinjury(P ＜ 0.05 or 0.01).Conclusion PARP inhibitor PJ34 can attenuate MMP-9 up-regulation,inhibit BBB injury and hence protect the brain against TBI in mice.