ABSTRACT
Objective To explore the diagnosis and treatment of non-tuberculosis mycobacteria (NTM) infection after cosmetic injection via scientific debridement surgery combined with regular application of anti-NTM drugs.Methods 14 patients who were infected with NTM after cosmetic injection and were not cured over a long period of time in other hospitals from 2012 to 2016.The patients were treated with VSD thorough surgical debridement,the bacterial type of NTM was identified by bacterial culture and PCR identification and anti-NTM drugs were systematically used according to the results of drug sensitivity.Results Fourteen patients who were treated with scientific debridement surgeries combined with regular anti-NTM drug treatment in our hospital for 2-4 months were discharged after their skin lesions were cleared and healed and they were continually treated with antiNTM drugs for 12 months.Fourteen patients were completely cured by using the above treatments without severe side effects,such as liver and kidney dysfunction,nervous system disorders and so on.Only colpitis mycotica occurred in 3 patients.In addition,one patient presented the decrease of leukopenia after using anti-NTM drugs for 2 months and continued to complete the treatment after we adjusted the treatment plan to returning the level of leukopenia to the normal.These 14 patients were followed up for 1-5 years with no recurrence of the lesion.The facial appearance of 12 patients were almost normal with slight scars.The facial surgery area of 2 patients were uneven and nearly recovered to normal facial appearance by tissue transplantation and photoelectric therapy.Conclusions For the NTM patients caused by invasive procedures such as injection,the comprehensive treatment program,which combined scientific debridement surgery and systematically targeted drug treatment,not only can effectively cure NTM infection,but also minimize secondary injury and restore the patients' appearance,which is worthy of clinical application.
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Aim To investigate Jaridonin′s selective killing of cancer cells and explore the related molecular mechanism. Methods After treatment by Jaridonin for 24 h, the effect of Jaridonin on the cell viability was examined using MTT assay. The effect of Jaridonin on cytomorphology and mitochondrial membrane poten-tial (Δψm) was observed by a fluorescence microsco-py. The apoptosis of cell lines treated with Jaridonin, as well as the level of reactive oxygen species ( ROS ) was analyzed by flow cytometry. Expression of the pro-teins related with mitochondria apoptosis pathways was detected by Western blot. Results Jaridonin caused strong antiproliferative and apoptotic effects on MGC-803 cells, but there were not remarkable effects on GES-1 cells. Furthermore, the expression of Bax was up-regulated, and the release of cytochrome c from mi-tochondria to cytosol was also promoted in MGC-803 cells treated by Jaridonin. The cleavage of caspase-3 in MGC-803 cells was also observed. Jaridonin increased persistently intracellular levels of ROS in MGC-803 cells, whereas the level of ROS in GES-1 rose in the first stage, and then decreased, and dropped to the basic level after 6 h. More interestingly, Jaridonin-in-duced ROS accumulation and the inhibition of MGC-803 cell proliferation were almost completely attenuated in the presence of GSH. Conclusions Jaridonin se-lectively kills cancer cells and induces apoptosis in MGC-803 through ROS-mediated mitochondrial dam-age.
ABSTRACT
<p><b>OBJECTIVE</b>The aim of this study was to explore the molecular mechanism of apoptosis in esophageal cancer cells induced by Isodon rubescens.</p><p><b>METHODS</b>The DNA-damage effect of Jaridonin was detected by single cell gel electrophoresis (SCGE). The p53 protein was determined by Western blot. GSH assay kit was employed to determine the GSH content in human esophageal cancer EC-1 cells. Intracellular levels of hydrogen peroxide (H2O2) or superoxide (O(2).-) were determined using the redox-sensitive probes 2', 7'-dichlorodihydrofluorescein diacetate (DCF) or dihydroethidium (DHE), and the fluorescence signal was assayed by fluorescence microscopy and by flow cytometry.</p><p><b>RESULTS</b>Jaridonin induced DNA damage in EC-1 cells remarkably. The olive tail moments (OTM) of control and 20, 40 µmol/L Jaridonin were 3.2, 45.2 and 89.0, respectively. Compared with the control, the differences were significant (P < 0.01 for both). Jaridonin resulted in extensive p53 up-regulation in the EC-1 cells. More importantly, the p53 up-regulation occurred as early as 2 h after Jaridonin incubation, and in a time-dependent manner (P < 0.05). p53 siRNA transfection inhibited apoptosis in the EC-1 cells, and the Jaridonin-induced apoptosis rate was reduced from 38.5% to 8.8%. Intracellular level of H2O2 was increased by Jaridonin, whereas the level of O(2).- was barely changed. The GSH content in EC-1 cells was reduced from (10.3 ± 1.6) nmol/mg protein to (4.6 ± 2.1) nmol/mg protein after 20 µmol/L Jaridonin incubation for 8 h, and it was further reduced with the increase of Jaridonin concentration. Jaridonin induced DNA damage, H2O2 accumulation and apoptosis were significantly attenuated in the presence of GSH, but Jaridonin showed little effect on normal human liver L-02 cells.</p><p><b>CONCLUSIONS</b>Jaridonin selectively induces apoptosis in esophageal cancer EC-1 cells through H2O2-mediated DNA damage by depleting GSH.</p>