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Objective: To evaluate the effect of irradiation of 60Co-γ on composition change of Curcuma Longa through HPLC fingerprint analysis and determination of curcumin content. Methods: An Agilent SB-C18 column (250 mm × 4.6 mm, 5 μm) was used as the column. Curcumin content was measured according to the method in 2015 edition of the “Pharmacopoeia of the People’s Republic of China”. Acetonitrile-0.1% phosphoric acid aqueous solution was used as the mobile phase of fingerprint analysis, and it was programmed in a gradient elution model and the detection wavelength was 240 nm. The effects of irradiation on content of curcumin and components change were analyzed by paired t-test and similarity evaluation. And then the comprehensive evaluation of constituent difference of C. Longa before and after irradiation was carried out by HCA and PCA analysis. Further more the stability of curcumin content and fingerprint similarity of three patches samples storage for 3 and 6 months was compared with that of 0 month. Results: There was no significant difference before and after irradiation for curcumin content (P > 0.05). The fingerprints of C. Longae were established and 16 peaks were identified as the common peaks. The similarity of each batch before and after irradiation was more than 0.998 and the same batch before and after irradiation have better clustering consistency. The changes of curcumin content for 3 and 6 months compared with 0 month was less than 5%, and the fingerprint similarity was all greater than 0.95. Conclusion: The established fingerprinting method is accurate and reliable. 60Co-γ irradiation has no significant effect on the curcumin content and chemical composition consistency of C. Longa, which did not affect its stability. It was a good way to evaluate the 60Co-γ irradiation effect on C. Longa by combining fingerprint analysis and the index components content determination. This method can provide reference for the utilization of irradiation on C. Longa.
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Objective To observe the effects of 2 Gy γ-ray irradiation on regulatory T cells (Tregs) and Th17 cells and immune balance of mice.Methods A total of fifty C57BL/6 male mice were randomly divided into two groups,the irradiated group exposed to 2 Gy of whole body γ-ray irradiation,and the control group sham-irradiated.At 1,3,7,14 and 28 d after radiation,changes of peripheral haemogram were detected respectively and Tregs in peripheral blood,thymus and spleen and Th17 cells in spleen were analyzed by flow cytometry.Results Compared with control group,the number of peripheral blood white cells (WBC) and lymphocyte in irradiated group reduced significantly post-irradiation (t =8.89-33.54,P ＜ 0.05),while the cell number of peripheral CD4 + CD25 + Tregs post-irradiation rose but not significantly.Thymic Treg cells increased 1 and 3 d post-irradiation(t =-6.45,-10.59,P ＜0.05),but reduced 28 d post-irradiation (t =5.34,P ＜ 0.05).Splenic Treg cells ascended obviously from 1 to 14 d post-irradiation (t =-6.82-3.89,P ＜ 0.05).After irradiation splenic Th17 cells increased at 1 d,and reached the maximal level at 3 d (t =-2.42,P ＜ 0.05),more obviously than splenic Treg cells.The reduction of Treg/Th17 ratio from 1 to 14 d post-irradiation disturbed Treg/Th17 balance and made it drift to the direction of Th17 (t =4.02-8.04,P ＜ 0.05).Conclusions Treg/Th17 imbalance plays an important role in immune injury induced by irradiation.
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Objective To evaluate the modification of C_(60) on the radiation effects of ~(60)Co-γ irradiation on zebrafish.Methods The adult and embryonic zebrafish were used as model organisms to examine the potential of C_(60) to elicit oxidative stress responses on the surviving rate,hatching rate and malformation occurrence,both upon exposure to light or in the dark.Reactive oxygen species (ROS) production and DNA damage were examined as the possible underlying mechanism.Results 500 × 10~(-9) nano-C_(60) waterborne exposure could enhance the γ-irradiation effects by decreasing adult fish survival upon light exposure,which resulted in ROS and DNA damage increasing.The hatching rates were also inhibited with higher malformation,though dark exposure did not make any enhancement,except that the 5000× 10~(-9) C_(60) would inhibit larvae hatching and induced more malformation.Conclusions Waterborne nano-C_(60) exposure may enhance the radiation effects on zebrafish,ROS production and DNA damage increasing may be the underlying mechanism.
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Objective To investigate the change of ATM phosphorylation in HepG2 cells following a condnuous low dose-rate irradiation.Methods Cells were pemistendy exposed to low dose-rate(8.28 cGy/h) irradiation.Indirect immunofluorescence and Western blot were used to detect the expression of ATM phosphorylated proteins.Colony forming assay Was used to observe the effect of a low dose-rate irradiation on HepG2 cell survival.Results After 30 min of low dose-rate irradiation.the phosphorylation of ATM occurred.After 6 h persistent irradiation,the expression of ATM phosphorylated protein reached the peak value,then gradually decreased.After ATM phosphorylation was inhibited with Wortmannin,the surviving fraction of HepG2 cells was lower than that of the irradiation alone group at each time point(P<0.05).Conclusions Continuous low dose-rate irradiation attenuated ATM phosphorylation.suggesting that continuous low dose-rate irradiation has a potential effect for increasing the radiosensitivity of HepG2 cells.
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Objective To investigate cadmium induced adaptive responses (AR) to either toxicant challenge or irradiation and also the role of PI3K family in the AR. Methods Cells were pre-treated with 0.1 or 1 μmol/L cadmium and then challenged by 50, 100 μmol/L cadmium or 1, 2 Gy γ-rays irradiation. Micronucleus induction was measured to evaluate the magnitude of AR. In some experiments, cells were treated with wortmannin during and after pretreatment. Results Cadmium of sub-lethal concentration could induce AR in all the cells toward 50 μmol/L cadmium or 1 Gy irradiation. When challenged by 50 μmol/L CdCl1, EM-C11 cells had an AR less apparent than the other two cell lines. Moreover, treatment of cells with wortmannin eliminated the AR in all three cell lines. Conclusions The magnitudes of AR in adapted cells may be related to multiple factors, such as DNA repair capacity, the priming and challenging dose of cadmium or irradiation. SSB rather than DSB repair is mainly involved in the cadmium induced AR and this cellular response may be mediated through ATM pathway.