ABSTRACT
Objective To explore the difference of cellular apoptosis levels in lungs between C 57BL/6J and C3H/HeN mice in the course of radiation induced pulmonary injury (RPI).Methods Sixty C57BL/6J mice and another sixty C3H/HeN mice were randomly divided into control group and irradiation group respectively .The 60 Co γray irradiation method was used to establish an RPI model with 20 Gy per irradiation.Lungs were obtained on 1 d, 3 d, 7 d, 1 month(m) and 3 m after irradiation, and then the apoptosis and expressions of γH2AX and AIF were detected by in situ terminal labeling and immunoblotting .Results 1 and 3 d after irradiation , many apoptotic cells , mainly apoptotic epithelial cells , could be seen in lungs and apoptotic cells in the lungs of C 57BL/6J mice outnumbered those of C3H/HeN mice.At one month after irradiation, there was no significant difference of cell apoptosis between these two groups of mice .Three months after irradiation, there were fewer apoptotic cells in lungs of C 57BL/6J mice than in C3H/HeN mice.C57BL/6J mice had a higher γH2AX expression in lungs than C3H/HeN mice did at 1 -7 days after irradiation.However, the expression ofγH2AX in lungs of C3H/HeN mice was higher than that of C57BL/6J mice at 3 m after irradiation.The expression of AIF in lungs of C3H/HeN mice was lower than that of C57BL/6J mice at 1 d, 3 d and 1 m,while the expression of AIF in lungs of C3H/HeN mice was higher than that of C57BL/6J mice at 3m after irradiation.Conclusion In the course of RPI, the occurence of DNA damage and cell apoptosis is different in lungs of C 57BL/6J mice and C3H/HeN mice.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the protection of silymarin against the human mesenchymal stem cell (MSC) apoptosis induced by serum deprivation and its underlying mechanism.</p><p><b>METHODS</b>Human umbilical cord MSCs were cultured in the absence of serum, and the silymain of different concentration (1-10 µg/ml) was added into the medium. MTT test was performed to observe the cell proliferation status. After being cultured for 72 hours, the cells were collected, and flow cytometry with Annexin-V-PI double-staining was used to detect the apoptotic cells from the control and silymarin-treated groups. Furthermore, the intracellular contents of BAX and BCL-2 were detected by Western blot for exploring the potential mechanism.</p><p><b>RESULTS</b>The silymarin promoted the proliferation of human UC-MSCs in a dose-dependent manner, reaching its maximal at a dose of 5 µg/ml. Moreover, silymarin could inhibit the serum deprivation-induced apoptosis of MSCs and, the inhibitory rate reached up to 30% when it was added at a concentration of 5 µg/ml. The content of intracellular BAX was obviously elevated after serum-deprivation treatment, and this increase could be blunted by the addition of silymarin. Meanwhile, the content of BCL-2 was not obviously changed.</p><p><b>CONCLUSION</b>The silymarin can stimulate MSC growth and inhibit the apoptosis of MSCs probably by the mitochondria pathway.</p>
Subject(s)
Humans , Apoptosis , Cell Proliferation , Culture Media, Serum-Free , Mesenchymal Stem Cells , Mitochondria , Proto-Oncogene Proteins c-bcl-2 , Metabolism , Silymarin , Pharmacology , Umbilical Cord , Cell Biology , bcl-2-Associated X Protein , MetabolismABSTRACT
This paper is aimed to study the effect of ADL on expression of β1-AR and M2-AchR in myocardial cells of rats exposed to microwave radiation. Immunohistochemistry, Western blot and image analysis were used to detect the expression of β1-AR and M2-AchR in myocardial cells at 7 and 14 d after microwave exposure. The results show that the expression level was higher in microwave exposure group and 0.75 g/(kg•d) ADL group than in sham operation group and significantly lower in 1.5 and 3.0 g/(kg•d) ADL groups than in microwave group. So we have a conclusion that the expression of β1-AR and M2-AchR is down-regulated in myocardial cells of rats exposed to microwave radiation. ADL can protect rats against microwave-induced heart tissue injury.