OBJECTIVE:To study the improving effects of argatroban on the brain damage of model rats with cerebral hemor-rhage. METHODS:50 SD rats were randomly divided into normal control group(equivalent normal saline),model group(equiva-lent normal saline),argatroban high,medium and low dose groups (0.75,1.5,3 mg/kg). All groups,except for normal control group,were reproduced models with cerebral hemorrhage,and the rats in each group were treated by corresponding drugs after 30 min,ip,once a day. The rats were executed after continuous administration for 3 days. The data was detected,including the con-tents of tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β),activity of cysteine-containing aspartic protease 3(Caspase-3), expressions of Bcl-2,Bax,matrix metalloproteinase-2(MMP-2)and MMP-9,and the phosphorylations of nuclear factor κB(NF-κB) p65 and IκBα. RESULTS:Compared with the normal control group,the contents of TNF-α and IL-1β,the activity of Cas-pase-3,the expressions of MMP-2,MMP-9 and Bax proteins were increased;the expression of Bcl-2 was decreased;and phos-phorylations of NF- κB p65 and IκBα in model group were increased,with significant differences(P<0.01). Compared with the model group,the contents of TNF-α and IL-1β,the activity of Caspase-3,the expressions of MMP-2,MMP-9 and Bax were de-creased;the expression of Bcl-2 was increased;and phosphorylations of NF-κB p65 and IκBα in argatroban low,medium and high dose groups were decreased,with significant differences (P<0.01 or P<0.05). And it was positively correlated with the dose. CONCLUSIONS:Argatroban has dose-dependent inhibition effects on the inflammatory cytokine secretion and apoptosis of brain tissue of model rats with brain hemorrhage,and the mechanism may be related to NF-κB signaling pathway.

In order to figure out phylogenetic relationship and genetic diversity of different geographical populations,genetic analyses of Aedes albopictus were performed based on mitochondrial gene COI.Based on samples collected from most distribution regions in China,mitochondrial gene Cytochrome C Oxidase Subunit I was obtained through PCR and DNA sequence.Together with some COI sequences downloaded from GenBank,60 COI sequences with the final length of 598 bp were used for subsequent analyses.Results showed that there was no obvious divergence according to phylogenetic analyse,all sequences were clustered together in Maximum Likelihood tree.Sixteen haplotypes were detected,and four of them shared haplotypes.Haplotype diversity (Hd) was 0.737,nucleotide diversity (π) was 0.20 ％.Population genetic differentiation analyses demon strated that Hainan population showed obvious divergences.In the network of haplotypes,H1 and H6 was found to be the primary haplotypes,and they formed two radical centers.All these results indicate that A.albopictus populations of China are expanding presently,and Hainan population become differential with other geographical populations,which probably attribute to geographical isolations.

The aim of the present study was to investigate the effects and possible mechanism of tetramethylpyrazine(TMP)on morphine-induced microglia activation and tolerance. The antinociception and morphine tolerance were assessed in mice using hot-water tail flick test. IBA-1(ionized calcium binding adapter molecule 1), the marker of microglia, was detected by immumofluorescence method. The expression of p-p38 MAPK and total p38 MAPK(mitogen-activated protein kinase, MAPK)was analyzed by Western blot; real-time polymerase chain reaction(RT-PCR)was used to detect the expression level of tumor necrosis factor-α(TNF-α)and interleukin-1β(IL-1β). Results showed that TMP(15, 30, 60 mg/kg, ip)inhibited morphine-induced up-regulation of IBA-1, p-p38, TNF-α and IL-1β in a dose-dependent manner, yet with no effect on the expression of total p38 MAPK. In conclusion, TMP significantly inhibited the activation of microglia evoked by morphine via p38 MAPK signaling pathway, thus attenuating morphine antinociception tolerance.

The cochlear auditory epithelium contains two types of sound receptors, inner hair cells (IHCs) and outer hair cells (OHCs). Mouse models for labelling juvenile and adult IHCs or OHCs exist; however, labelling for embryonic and perinatal IHCs or OHCs are lacking. Here, we generated a new knock-in Fgf8^P2A-3×GFP/+ (Fgf8^GFP/+) strain, in which the expression of a series of three GFP fragments is controlled by endogenous Fgf8 cis-regulatory elements. After confirming that GFP expression accurately reflects the expression of Fgf8, we successfully obtained both embryonic and neonatal IHCs with high purity, highlighting the power of Fgf8^GFP/+. Furthermore, our fate-mapping analysis revealed, unexpectedly, that IHCs are also derived from inner ear progenitors expressing Insm1, which is currently regarded as an OHC marker. Thus, besides serving as a highly favorable tool for sorting early IHCs, Fgf8^GFP/+ will facilitate the isolation of pure early OHCs by excluding IHCs from the entire hair cell pool.
Animals ; Mice ; Hair Cells, Auditory, Inner ; Cochlea/metabolism* ; Hair Cells, Auditory, Outer/metabolism* ; Disease Models, Animal ; Fibroblast Growth Factor 8/metabolism*