To investigate the effect of angiotensin II and angiotensin1-7 on alpha-smooth muscle actin (alpha-SMA)-induced Ca(2+)-independent pathways mediated by Rho kinase2 in hepatic stellate cells (HSCs).

To observe the effect of Shuanghuanglian injection on cerebral expression of nuclear factor-kappaB (NF-kappaB) in mice with viral encephalitis.

To evaluate the effect of bone morphogenic protein 7 (BMP-7) on nephrin expression and distribution in diabetic rat kidneys.

To investigate the changes in angiotensinogen (AGT), angiotensin II type 1 receptor (AT(1)R), endothelial nitric oxide synthase (eNOS) mRNA and protein expressions and nitric oxide (NO) content in the rat glomeruli in response to leptin stimulation.

To investigate the effect of sinomenine on the expression of chemokines and chemokine receptors of dendritic cells in patients with rheumatoid arthritis in vitro.

To investigate the effect of vasoactive intestinal peptide (VIP) on angiogenesis after focal cerebral ischemia.

The bioaccumulation regulation and the toxicity of diethylstilbestrol (DES) were studied on zebrafish (Danio rerio) embryos with the methods of HPLC and early life stage test, and the toxic mechanisms were also discussed with the techniques of quantitative structure-activity relationship (QSAR) and gene chips. After the zebrafish embryos exposed at 0.2 mg x L(-1) DES for 24, 48 and 72 h, the body levels of DES in zebrafish embryo were (25.78 +/- 4.95), (54.88 +/- 7.10) and (71.93 +/- 10.55) microg/g, respectively. Even exposure started at different time (0 hpf and 8 hpf), the most sensitive sub lethal endpoints were both 72 h delayed hatch, and the EC50 values for them were (0.14 +/- 0.09) and (0.33 +/- 0.14) mg/L, so that zebrafish embryo was more sensitive to the exposure of DES before the stage of gastrula (8 h after fertilization). QSAR studies found when compared with other phenol-endocrine disrupts, DES was much more toxic, and this related to its higher TE value (52.1217 eV). Meanwhile, when adult zebrafish exposed at 5 microg/L DES for 21 d, it was found by the gene chips that parts of gene expressions would be changed and the genetic toxicity of DES was approved. DES was concluded to be developmental and genetic toxic to zebrafish, and the biochemical reaction-associated process might be the key parameter in determining the toxicity level.

In order to investigate the possible mechanism of its function to degrade lipid, we detect the effects of hawthorn flavanone to the influence on blood-fat levels and adipogenesis genes transcription expression in fat and muscle tissue of hyperlipoidemia mouse.

To investigate the dynamic changes in angiogenesis within the tumor tissue of mice bearing S180 tumor at different day-points of oral administration with a Chinese medicine compound "Yiliuyin" (YLY) and to explore the anti-tumor mechanisms of YLY in vivo.

To study the effect of Astragalus mongholicus (AM) on the expression of transforming growth factor-beta1 (TGF-beta1) in SD rats with unilateral ureteral occlusion (UUO) and to elucidate the mechanisms underlying the renoprotective effects of AM.

To study the effect of tanshinone II A (TSN) on angiotensin II (Ang II) induced proliferation of vascular smooth muscle cells (VSMCs).

To investigate the anticancer effects of Erbie San on the rats bearing Walker-256 liver cancer and the potential mechanism of its angiogenesis effects.

To study effect and mechanisms of tetramethylpyrazine (TMP) on renal interstitial fibrosis induced by unilateral ureteral obstruction in rats.

To investigate the effect of dauricine on the apoptosis of neuronal cells and the expression of apoptosis-related proteins in the brain penumbra of rats induced by transient focal cerebral ischemia-reperfusion injury.

To examine inhibition action of multi-glycoside of Tripterygium wilfordii (GTW) on infiltration of inflammatory cell in glomeruli with anti-Thy1.1 glomerulonephritis (anti-Thy1.1 GN), and to clarify its effects on inflammatory in vitro.

The aim of this study was to investigate the regulation of 5-aza-CdR on transcription of SHP-1 gene and effects on the proliferation and apoptosis of K562 cells. Methylation-specific PCR (MSP) was used to detect CpG island methylation in SHP-1 promoter. MTT and flow cytometry were used to detect the growth and apoptosis of K562 cells after treatment with different concentration of 5-aza-CdR. The expressions of SHP-1 mRNA and protein were determined by FQ-PCR and Western blot. The expression of p-JAK2 was assayed by Western blot. The result showed that methylation of SHP-1 gene promoter was detected in K562 cells, and the SHP-1 mRNA and protein were expressed again in K562 cells after treatment with 5-aza-CdR, meanwhile the expression of phosphorylated P-JAK2 was down-regulated; 5-aza-CdR significantly inhibited the cell growth in dose and time dependent manners. AG490 inhibited the cell proliferation. 5-aza-CdR increased the apoptosis rate of K562 cells also in dose- and time-dependent manners. The apoptosis rates of K562 cells treated with 5-aza-CdR for 1, 3 and 5 days were 9.3%, 24.2% and 37.7% respectively. After treatment with 2 micromol/L 5-aza-CdR for 24 hours, cells in G(0)/G(1) phase increased gradually, cells in G(2)/M phase decreased gradually, cells were arrested in G(0)/G(1) phase. The cell ratios in G(2)/M phase at 1, 3 and 5 days after treatment with 5-aza-CdR were 30.7%, 23.45 and 19.3% respectively. It is concluded that the 5-aza-CdR, inhibitor of specific methylation transferase, can re-express the silent SHP-1 gene in K562 cells, inhibits the proliferation of leukemia cells and induces cell apoptosis by activating JAK/STAT pathway.

To observe the effect of Tanshinone II A on the expression of epidermal growth facter (EGF) and epidermal growth facter recepter (EGFR) in human hepatocellular carcinoma cell line SMMC-7721.

To investigate the antagonism of LY333531 on the increased permeability of cardiac microvascular endothelial cells (CMECs) induced by high glucose.

To investigate molecular mechanism of tanshinone II A inducing differentiation and apoptosis in acute promyelocytic leukemia NB4 cells.

To observe the contribution of Qingnao drop pilula to the alteration of myristoylated alanine-rich C kinase substrate (MARCKS) mRNA expression in acute multi-infarction hippocampus.