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This study aims to investigate the effect of Buyang Huanwu Decoction on blood flow recovery and arteriogenesis after hindlimb ischemia in mice via the platelet-derived growth factor(PDGF) signaling pathway. Forty C57BL/6 mice were randomized into model(clean water, 10 mL·kg~(-1)·d~(-1)), beraprost sodium(positive control, 18 μg·kg~(-1)·d~(-1)), and low-, medium-, and high-dose(10, 20, and 40 g·kg~(-1)·d~(-1), respectively) Buyang Huanwu Decoction groups(n=8). The hindlimb ischemia model was established by femoral artery ligation. The mice were administrated with corresponding agents by gavage daily for 14 days after ligation. For laser Doppler perfusion imaging, the mice were anesthetized and measured under a Periscan PSI imager. The density of capillary and arterio-le in the ischemic gastrocnemius was measured using immunofluorescence staining of the frozen tissue sections. Western blot was employed to determine the expression of PDGF subunit B(PDGFB), phosphorylated mitogen extracellular kinase(p-MEK), MEK, phosphorylated extracellular signal-regulated kinase(p-ERK), and ERK. Real-time PCR was employed to determine the mRNA level of PDGFB. The Buyang Huanwu Decoction-containing serum was used to treat the vascular smooth muscle cells(VSMCs) in hypoxia at doses of 10% and 20%. The proliferation and migration of VSMCs was assessed in vitro. The results showed that compared with the model group, beraprost sodium and Buyang Huanwu Decoction enhanced the blood flow recovery, increased the capillary and arteriole density, and up-regulated the protein levels of PDGFB, p-MEK, p-ERK, and mRNA levels of PDGFB, with the medium-dose Buyang Huanwu Decoction demonstrating the most significant effect. The 10% Buyang Huanwu Decoction-containing serum enhanced the proliferation and migration of VSMCs. Our findings demonstrate that Buyang Huanwu Decoction up-regulates PDGFB transcription and activates PDGF signaling pathway to promote arteriogenesis and blood flow recovery in ischemic gastrocnemius.

The model compound [Zn(HCOO)2(4,4'-bipy)] (1; 4,4'-bipy = 4,4'-bipyridine) is selected in this work to demonstrate the effectiveness of our previously proposed design strategy for electron-transfer photochromic metal-organic complexes. The electron-transfer photochromic behavior of 1 has been discovered for the first time. Experimental and theoretical data illustrate that the photochromism of 1 can be attributed to the electron transfer from formato to 4,4'-bipy and the formation of a radical photoproduct. The electron transfer prefers to occur between formato and 4,4'-bipy, which are combined directly by the Zn(II) atoms. A high-contrast (up to 8.3 times) photoluminescence switch occurs during the photochromic process. The similarity of photochromic behaviors among 1 and its analogues as well as viologen compounds has also been found. Photochromic studies of this model compound indicate that new electron-transfer photochromic metal-organic complexes can be largely designed and synthesized by the rational assembly of nonphotochromic electron-donating and electron-accepting ligands.

LC-based tunable filter with large aperture has been developed utilizing the effect of electric controlled birefringence. Spectral test indicated that this filter can operate in the visible band with an average 20 nm FWHM. A small scale spectral imaging system was established based on this tunable filter. Spectral imaging experiments on a certain number of samples show that this system can be tuned continuously with random-access selection of any wavelength, and has a higher level of resolving power in respect of both imaging and spectral tuning in the visible band, which has a brilliant application potentiality in biology, iatrology, environmental protection, resource detection through hyper-spectral imaging or ultra-spectral imaging.

Objective: To reverse the multidrug resistant (MDR) phenotype of human breast carcinoma cells by small hairpin RNA (shRNA) technique targeting hypoxia-inducible factor (HIF)-1alpha gene., Methods: Small hairpin RNA (shRNA) eukaryotic expression vector targeting HIF-1alpha gene, named pSilencer-HIF, was constructed and transfected into MCF-7/ADR human breast cancer cells by liposome technique. Tumor cell livability (TCL) and Rhodamine 123 efflux assay were used to monitor the biological changes of the transfected cells. The mRNA and protein expression of HIF-1alpha and mdr-1 were investigated by RT-PCR and Western blot., Results: The successful construction of pSilencer-HIF plasmid was confirmed by DNA sequencing. HIF-1alpha mRNA and protein levels were significantly decreased in MCF-7/ADR cells after the transfection and there was a direct correlation between HIF-1alpha and mdr-1 expression. By comparing the cells transfected with control vector and the MCF-7/ADR cells transfected with pSilencer-HIF, a reduced TCL from 76% to 43%, and an increased Rhodamine 123 fluorescence intensity from 22.0% to 86.6% were observed., Conclusions: pSilencer-HIF-1alpha has been successfully constructed. The inhibition of HIF-1alpha expression through shRNA technique can significantly reverse the multidrug resistance phenotype of MCF-7/ADR cells.

Objective: To assess the role of methylated mismatch repair (MMR) genes (hMLH1, hMSH2 and hMSH3) in the carcinogenesis and progression of hepatocellular carcinoma (HCC)., Methods: Samples of 38 cases of HCC along with their corresponding noncancerous tissues, 2 samples of donated normal tissue and 6 cell lines were collected and subject to the methylation-specific PCR (MSP) to examine promoter methylation status of MLH1, MSH2 and MSH3. Six tumor cell lines were analyzed before and after 5-aza-2'-deoxycytidine treatment. In addition, alterations of mRNA expression of MMRs were investigated by quantitative reverse transcription-PCR., Results: CpG island methylation of hMLH1 and hMSH2 was observed in 13.2% (5 of 38 samples) and 68.4% (26 of 38 samples) respectively in HCC, 2.6% (1 of 38 samples) and 55.3% (21 of 38) respectively in corresponding noncancerous tissues, but not in normal control tissues. Promoter methylation of the hMSH2 gene was present in 83.3% of cell lines tested (5/6), but none were observed for the hMLH1 gene. Promoter methylation of the hMSH3 gene was not identified in any tissue samples or cell lines. After 5-aza-2'-deoxycytidine treatment, hMSH2 methylation was induced or completely reversed, and its mRNA expression was increased in most cell lines., Conclusions: Our results suggest that promoter hypermethylation of hMLH1 and hMSH2 genes is common in HCC. Particularly, there is a high frequency of methylation of hMSH2 in both cancer and noncancerous tissues, but not in normal control tissue. Therefore, hypermethylation of MMR genes, especially hMSH2, may be involved in the carcinogenesis of HCC and may serve as an early diagnostic marker for HCC. The close correlation between hMSH2 methylation and low expression of its mRNA suggests that hMSH2 methylation is an important pathway in the regulation of gene expression.

Objective: To study the reversing effect of Grape seed polyphenol (GSP) on multidrug resistance of MCF-7/ADR cell in vivo., Methods: The transplantable breast carcinoma cell line MCF-7/ADR model was established in BALB/C-nu/nu mice by subcutaneous implantation. Flow cytometry (FCM) was used to investigate the changes of Pgp expression and apoptosis rate after different drug treatment., Results: GSP has some effect on inhibition of tumor growth (the rate of inhibition was 18.35%), and combined with adriamycin can significantly inhibit tumor growth in nude mice, 20 mg/kg GSP can effectively reverse the resistance of MCF-7/ADR cells to ADR in vivo, and the rate of inhibition was 54.64%. FCM results showed that the expression of Pgp was significantly decreased (32.03 +/- 2.09) After administration of GSP and ADR, there was distinct difference between it and control (55.13 +/- 2.12). The mean rate of apoptosis was 15.12% +/- 1.04%, and was significantly increased compared with control (9.07% +/- 0.43%), P < 0.05., Conclusion: GSP can effectively reversed the resistance of MCF-7/ADR cells in nude mice, the mechanism may be correlated with inhibition of Pgp expression and apoptosis.