Objective To explore the radiosensitivity of berberine on esophageal cancer cells under hypoxia condition.Methods MTT assay and clonogenic survival assay were used to evaluate the effect of berberine on proliferation inhibition and radiosensitivity of esophageal cancer cells,respectively.Immunofluorescence was employed to examine the expression of HIF-1.The change of cell cycle distribution and cell apoptosis was assayed by flow cytometry.The expression of HIF-1 was measured by Western blot.DNA damage was detected by γ-H2AX Foci counting.Results With a clear dose and time effect,berberine inhibited cell proliferation and enhanced cell radiosensitivity(t =3.69,P＜0.05)with a sensitizing enhancement ratio(SER)of 1.42.Berberine caused a dose-dependent decrease in HIF-1 protein expression and also significantly increased the cell apoptosis in ECA-109 population(t=4.74,P＜0.05).Compared with the radiation alone group,berberine enhanced X-ray induced DNA double chain breaks(DSB).Conclusions Berberine can increase the radiosensitivity of esophageal cell line ECA-109,which may be associated with decrease of HIF-1 expression and induction of apoptosis in ECA-109 cells.

A chimeric protein called Wallerian degeneration slow (Wld(S)) was first discovered in a spontaneous mutant strain of mice that exhibited delayed Wallerian degeneration. This provides a useful tool in elucidating the mechanisms of axon degeneration. Over-expression of Wld(S) attenuates the axon degeneration that is associated with several neurodegenerative disease models, suggesting a new logic for developing a potential protective strategy. At molecular level, although Wld(S) is a fusion protein, the nicotinamide mononucleotide adenylyl transferase 1 (Nmnat1) is required and sufficient for the protective effects of Wld(S), indicating a critical role of NAD biosynthesis and perhaps energy metabolism in axon degeneration. These findings challenge the proposed model in which axon degeneration is operated by an active programmed process and thus may have important implication in understanding the mechanisms of neurodegeneration. In this review, we will summarize these recent findings and discuss their relevance to the mechanisms of axon degeneration.
Animals ; Axons ; physiology ; Humans ; Mice ; Mice, Mutant Strains ; Models, Neurological ; Mutant Proteins ; genetics ; physiology ; Mutation ; NAD ; biosynthesis ; Nerve Degeneration ; etiology ; genetics ; physiopathology ; Nerve Tissue Proteins ; genetics ; physiology ; Nicotinamide-Nucleotide Adenylyltransferase ; genetics ; physiology