ABSTRACT
@#<b>Objective</b> To investigate the changes of chromosome aberration and micronucleus frequencies in the peripheral blood of patients with cancer before and after treatment, and to provide a basis for clinical prevention and treatment. <b>Methods</b> We collected the physical examination data of 102 patients with cancer before and after treatment from 2016 to 2021 to analyze the changes of chromosome aberration and micronucleus frequencies in peripheral blood. <b>Results</b> Before and after treatment, there were significant differences in chromosome aberration frequency and micronucleus frequency in peripheral blood lymphocytes in patients having radiotherapy or chemoradiotherapy (all <i>P</i> < 0.05), but no significant difference was observed in either index for patients having chemotherapy (both <i>P</i> > 0.05). Before and after radiotherapy, there were significant differences in the numbers of patients with abnormal chromosome aberration frequency and those with abnormal micronucleus frequency in lymphocytes (both <i>P</i> < 0.001). Before and after chemotherapy, there was no significant difference in the number of patients with abnormal chromosome aberration frequency (<i>P</i> = 0.100) or those with abnormal micronucleus frequency (<i>P</i> = 0.110). <b>Conclusion</b> Radiotherapy can cause abnormalities in chromosome aberration and micronucleus frequencies in peripheral blood lymphocytes, which can be useful for monitoring radiotherapy injury to formulate effective emergency plans and evaluate radiation dose in each course of treatment.
ABSTRACT
Amyloid β-protein(Aβ) deposition in the brain is directly responsible for neuronal mitochondrial damage of Alzheimer's disease(AD) patients. Mitophagy, which removes damaged mitochondria, is a vital mode of neuron protection. Ginsenoside Rg_1(Rg_1), with neuroprotective effect, has displayed promising potential for AD treatment. However, the mechanism underlying the neuroprotective effect of Rg_1 has not been fully elucidated. The present study investigated the effects of ginsenoside Rg_(1 )on the autophagy of PC12 cells injured by Aβ_(25-35) to gain insight into the neuroprotective mechanism of Rg_1. The autophagy inducer rapamycin and the autophagy inhi-bitor chloroquine were used to verify the correlation between the neuroprotective effect of Rg_1 and autophagy. The results showed that Rg_1 enhanced the viability and increased the mitochondrial membrane potential of Aβ-injured PC12 cells, while these changes were blocked by chloroquine. Furthermore, Rg_(1 )treatment increased the LC3Ⅱ/Ⅰ protein ratio, promoted the depletion of p62 protein, up-regulated the protein levels of PINK1 and parkin, and reduced the amount of autophagy adaptor OPTN, which indicated the enhancement of autophagy. After the silencing of PINK1, a key regulatory site of mitophagy, Rg_1 could not increase the expression of PINK1 and parkin or the amount of NDP52, whereas it can still increase the LC3Ⅱ/Ⅰ protein ratio and promote the depletion of OPTN protein which indicated the enhancement of autophagy. Collectively, the results of this study imply that Rg_1 can promote autophagy of PC12 cells injured by Aβ, and may reduce Aβ-induced mitochondrial damage by promoting PINK1-dependent mitophagy, which may be one of the key mechanisms of its neuroprotective effect.