Objective To observe the protective effect of anthocyanin on irradiation induced bone marrow c-kit positive cell injury, and further explore its possible mechanism. Methods Mouse bone marrow c-kit positive cells were collected by cell sorting method. There were 2 groups: control group and anthocyanin group, which were sub-divided into three groups and received 0 Gy, 1 Gy and 4 Gy irradiation respectively. The control group was added 700μL cell suspension and an equal volume of serum-free hematopoietic stem/progenitor cell culture medium. The 2 × 10-5 mol/L anthocyanin was co-cultured with mouse bone marrow c-kit positive cells of anthocyanin group half an hour before irradiation exposure, then cells were cultured for 18 hours under the conventional culture conditions (37℃,5%CO2). Mouse c-kit positive cell viability was measured by bioluminescence, and which was reflected by relative light units (RLU). The ability of colony-forming units was reflected by CFU-GM. The reactive oxygen species (ROS) level and mean fluorescence intensity (MFI) ofγ-H2AX were detected by flow cytometry. Results Compared to un-irradiated control group, the cell viability and the number of CFU-GM were decreased significantly, while the ROS level and MFI ofγ-H2AX were increased in c-kit positive cells irradiated with 1 Gy and 4 Gy (P<0.05). Compared to 1 Gy and 4 Gy irradiation groups, c-kit positive cell viability and the number of CFU-GM were increased, the ROS level and MFI of γ-H2AX were decreased in anthocyanin group (P < 0.05). Conclusion Anthocyanin exhibits a promising protective effect on radiation-induced bone marrow c-kit positive cell injury, which may be related to the alleviating ROS and DNA damage in bone marrow cells.

To investigate the effects of Yupingfeng granule (YPF) on immune factors of the rats with allergic rhinitis (AR) induced by ovalbumin(OVA). OVA 0.3 mg, Al(OH)3 30 mg and saline 1 mL were mixed and intraperitoneally injected for the initial immunization, 4% OVA 200 μg (50 μL) was given to the nose on the 15th day for the second immunization to establish the allergic rhinitis model. Sixty male SD rats were randomly divided into allergic rhinitis(AR) model group, Yupingfeng granule three dose (2.7,1.35,0.68 g•kg⁻¹) groups, control drug Biyankang (0.4 g•kg⁻¹) and normal control group. After 14 days, efforts were made to collect blood from abdominal aorta, and take nasopharynx tissues and fasten them into 10% formaldehyde for a pathological examination. The levels of HIS, IgE, IL-4 and TNF-α in serum were examined by radioimmunoassay, and nasal mucosa tissues were examined by HE staining. According to the results, the levels of HIS, IgE, IL-4 and TNF-α in serum of Yupingfeng granule groups were significantly lower than that of AR model group (P<0.05, P<0.01). Nasal mucosa tissues showed slight morphological changes and inflammatory cell infiltration, with unobvious necrosis. Yupingfeng granule can improve the pathological changes of nasal mucosa tissues, and reduce the production and release of immune factors during allergic rhinitis (AR) process in vivo by OVA, which may be the important curative mechanism of allergic rhinitis.

OBJECTIVE To investigate the effects of aucubin （AU） on the proliferation and tumor growth of prostate cancer （PC） cells by regulating the protein kinase B （Akt）/murine double minute2 （MDM2）/p53 signaling pathway. METHODS Prostate cancer cell PC3 were separated into control group， 50 μmol/L AU group， 100 μmol/L AU group， SC79 （Akt activator） group （5 μmol/L）， and 100 μmol/L AU+SC79 group. The cell cloning and proliferation ability were investigated； the rate of cell apoptosis and the expressions of Akt/MDM2/p53 signaling pathway-related protein were detected. Meanwhile， xenograft tumor models of nude mice were constructed and separated into tumor group， AU group （80 mg/kg）， SC79 group （50 mg/kg）， and AU+SC79 group （80 mg/kg AU+50 mg/kg SC79）， with 10 mice in each group. They were given relevant medicine， once a day， for 21 d. After the last medication， tumor weight was determined， and the expressions of nucleus-associated antigen （Ki-67） and Akt/MDM2/p53 signaling pathway-related protein were detected in tumor tissue. RESULTS In the cell experiment， compared with control group， the cell clonal formation number， proliferation rate and phosphorylation levels of Akt and MDM2 protein in 50 μmol/L AU and 100 μmol/L AU groups were significantly decreased （P＜0.05）， while the cell apoptosis rate and p53 protein expression levels were significantly increased （P＜0.05）； however， the change trend of each index in SC79 group was opposite （P＜0.05）. Compared with 100 μmol/L AU group， the cell clonal formation number， proliferation rate and phosphorylation levels of Akt and MDM2 protein in 100 μmol/L AU+SC79 group were significantly increased （P＜0.05）， while cell apoptosis rate and p53 protein expression levels were significantly decreased （P＜0.05）； however， compared with SC79 group， the changing trend of indexes was the opposite （P＜0.05）. In the in vivo experiment， compared with the tumor group， the tumor mass and Ki-67 positive expression and the phosphorylation levels of Akt and MDM2 protein in nude mice of AU group were significantly decreased （P＜0.05）， and the expression level of p53 protein was significantly increased （P＜0.05）， but the changing trend of above indexes of nude mice in SC79 group were opposite （P＜0.05）. Compared with AU group， the tumor mass， Ki-67 positive expression and phosphorylation levels of Akt and MDM2 protein in tumor tissues of nude mice in AU+SC79 group were significantly increased （P＜0.05）， while the expression level of p53 protein was significantly decreased （P＜0.05）； however， compared with SC79 group， the changing trend of above indexes was opposite （P＜0.05）. CONCLUSIONS AU can inhibit PC cell proliferation and tumor growth by inhibiting Akt/MDM2/p53 signaling pathway.

Objective To investigate the radiosensitization effects and mechanisms of novel benzothiadiazole derivatives HL-095 to KRAS-mutant non-small cell lung cancer ( NSCLC ) H358 , A549 , and H460 cell lines . Methods The benzothiadiazole derivative HL-095 was designed and synthesized with AZD6244 as the lead compound. The ability of HL-095 to inhibit the activity of MEK kinase was detected by the mitogen-activated extracellular signal-regulated kinase 1 (MEK1). H358, A549 and H460 cells were inoculated and cultured at appropriate density, and divided into control group, HL-095 group, irradiation group and HL-095 combined irradiation group. One-time irradiation with 137Cs gamma rays was used with a dose rate of 1.02 Gy/min. The expression of phosphorylated extracellular regulatory protein kinase ( p-ERK ) in H358 , A549 and H460 cells was detected by Western Blot. The cell proliferation was detected by cloning assay. The degree of DNA damage was analyzed by Comet assay. The G2/M phase cells were detected by flow cytometry. The level of the checkpoint kinase 1 (CHK1) protein and its phosphorylation in A549 and H358 cells was detected by Western Blot. Results HL-095 can inhibit the activity of MEK1. Compared with the control group, the expression levels of p-ERK protein of H358, A549, and H460) cells in HL-095 group were decreased, the percentages of cells in the G2/M phase were also decreased, and the differences were statistically significant (all P<0.01). The expression and phosphorylation of CHK1, a key protein of DNA damage repair, was down-regulated in A549 and H358 cells. Compared with the irradiated group, the proliferation of the three kinds of cell in HL-095 combined irradiation group was inhibited, the DNA damage was more serious, the Olive tail moment, tail length, tail length and tail DNA percentage were significantly increased, and the differences were statistically significant (all P<0.05). Conclusion As a MEK inhibitor, the novel benzothiadiazole derivative HL-095 can enhance the radiosensitivity of KRAS mutant NSCLC cells by inhibiting DNA damage repair and reducing G2/M arrest.

AIM: To find specific metabolic markers for women entering peri-menopausal period and patients with menopausal syndrome based on