Lutein inhibits tumor progression through the ATR/Chk1/p53 signaling pathway in non-small cell lung cancer.

Lung cancer is the leading cause of cancer-related death. In particular, non-small cell lung cancer (NSCLC) accounts for approximately 85% of all lung cancer cases. Due to tumor resistance and the toxicity of chemotherapeutic agents, it is increasingly critical to discover novel, potent antitumorigenic drugs for treating NSCLC. Lutein, a carotenoid, has been reported to exert toxic effects on cells in several tumor types. However, the detailed functions and underlying mechanisms of lutein in NSCLC remain elusive. The present study showed that lutein significantly and dose-dependently inhibited cell proliferation, arrested the cell cycle at the G0/G1 phase, and induced apoptosis in NSCLC cells. RNA-sequencing analysis revealed that the p53 signaling pathway was the most significantly upregulated in lutein-treated A549 cells. Mechanistically, lutein exerted antitumorigenic effects by inducing DNA damage and subsequently activating the ATR/Chk1/p53 signaling pathway in A549 cells. In vivo, lutein impeded tumor growth in mice and prolonged their survival. In conclusion, our findings demonstrate the antitumorigenic potential of lutein and reveal its molecular mechanism of action, suggesting that lutein is a promising candidate for clinical NSCLC treatment.

[Mechanism underlying photocatalyzed degradation of methyl orange by layered black phosphorus]. / é»‘ç£·çº³ç±³ç‰‡å ‰å‚¬åŒ–ç”²åŸºæ©™é™è§£æœºç†.

A large amount of azo dye wastewater is discharged into the environment, with serious risks to ecosystems and human health. Therefore, the development of treatment technology of azo dye wastewater was of practical significance. Photocatalytic methods showed promising application prospects due to easy to implement and effective. In this study, layered black phosphorus nanosheet (LBP) was used as a catalyst through liquid phase exfoliation method. Methyl orange (MO) was employed as a model azo dye to investigate the catalytic mechanism of LBP. The dominant transient species involved in the photocatalytic reaction was probed by quenching and fluorescence probe experiments. Degradation pathways of MO were proposed according to degradation products identified by the liquid chromatography-mass spectrometry. The results showed that degradation rate (kobs) of MO at acidic condition (pH=3.0) or alkaline condition (pH=11.0) was higher than that at neutral condition (pH=7.0). Degradation pathways of MO included that the azo bond was attacked by hydroxyl radicals (·OH) photogenerated by the LBP, and the intermediate products were further oxidized by ·OH to produce N, N-dimethyl-4-(2-p-phenylmethylhydrazine) aniline, 2-(dimethylamino)-5-((4(dimethylamino) phenyl) diazenyl) phenol and N, N-dimethyl-4-nitroaniline.

[Effects of Crude Atractylodis Rhizoma and Processed Atractylodis Rhizoma on AQP1 - AQP5 and Hemorheology in Healthy Rats].

OBJECTIVE: To study the different effects of crude Atractylodis Rhizoma and processed Atractylodis Rhizoma in healthy rats, in order to prove the traditional theory that the crude Atractylodis Rhizoma has dry effects and the dry effects can be weaken by processing. METHODS: Health rats had been orally administered with pure water, crude Atractylodis Rhizoma, processed Atractylodis Rhizoma and atropine. The concentration of AQP1 and AQP5 in submaxillary gland were measured by ELISA. Their index of submaxillary gland, hemorheology and moisture content of intestine were also measured. RESULTS: There were obvious differences of concentration of AQP1 and AQP5 in submaxillary gland, index of submaxillary gland, hemorheology and moisture content of intestine between the rats which had been orally administered crude Atractylodis Rhizoma and the rats administered processed Rhizoma Atractylodes. CONCLUSIONS: The dry effects of Atractylodis Rhizoma works on rats' moisture content of intestine, index of submaxillary gland and hemorheology. The dry effects can be weaken by processing.

[The effect of fluoride on the metabolism of teeth and bone in rats].

PURPOSE: To investigate the effect of fluoride on the metabolism of teeth and bone in rats, and to probe the mechanism of pathogenesis of dental fluorosis. METHODS: A total of 48 Wistar rats were randomly and equally divided into 4 groups including control group (distilled water), low-dose group(NaF,50 mg/L), medium-dose group (NaF,100 mg/L) and high-dose group (NaF, 150 mg/L). After 8 weeks, the rats were sacrificed under anesthesia, and serums were collected. The biochemical technique was used to test serum calcium. Changes in the fluorine content in serums and teeth of each group were analyzed with fluoride ion selective electrode method. Radioimmunoassay was employed to detect the levels of osteocalcin (OC), parathormone (PTH) and calcitonin (CT), respectively. SPSS13.0 software package was used for statistical analysis. RESULTS: The fluorine content in serum and teeth in the fluoride group were significantly higher than that of the control group (P<0.05), and increased with the increasing concentrations (F value was 11.234 and 275.148 respectively, P<0.01). The level of calcium in serum (F=3.906, P<0.05) in the fluoride group was significantly lower than in the control group. The level of PTH and OC in serum in medium and high-dose group were significantly higher than in the control group (P<0.01), with the level of CT in high-dose group decreased significantly (P<0.01). The differences of the level of OC, PTH, CT between groups were significant (F value was 8.548, 3.801 and 5.121 respectively, P<0.05). CONCLUSIONS: Fluoride affects the metabolism of teeth and bone in rats and OC, PTH, CT plays a key role in the pathogenesis of dental fluorosis.