Objective To investigate the effect of protein phosphate 4 ( PP4) activation on hepatocyte lipoapoptosis. Methods HepG2 cells were treated with 400 μmol / L palmitic acid (PA) for 24 hours to establish hepatocyte lipoapoptosis model. C57BL / 6J mice were fed with Western diet for 16 weeks to establish non-alcoholic steatohepatitis (NASH) model. The PP4 dominant negative mutant adenovirus vector AD-PP4RL was constructed. HepG2 cells were transfected with AD-PP4RL adenovirus to inhibit the activity of PP4 in hepatocytes. Mice were intravenously injected through the tail vein with AD-PP4RL adenovirus to inhibit the activity of PP4 in the liver. HepG2 cells were transfected with RAC1 lentivirus to inhibit the expression of RAC1. The lipid accumulation was detected by BoDIPY staining in cells and tissues. The levels of apoptosis were detected by TUNEL staining. The activity of PP4 was determined by immunoprecipitation combined with serine-threonine phosphatase activity assay kit. The activity of RAC1 was detected by GTPase activity assay kit. The expression levels of lipid metabolism and lipid apoptosis related proteins were detected by Western blotting. Results ① The activity of PP4 was increased in HepG2 cells treated with PA and in the livers of NASH mice induced by Western diet. ② The overexpression of dominant negative mutant adenovirus vector AD-PP4RL inhibited the activity of PP4 effectively. ③ Inhibition of PP4 activity decreased the level of lipoapoptosis in PA-treated HepG2 cells and livers of NASH mice, as well as the expression levels of lipoapoptosis related genes such as PUMA, Bim and c-caspase3. ④ RAC1 mediates the role of PP4 in hepatocyte lipoapoptosis. Conclusion Inhibition of PP4 activity alleviates hepatocyte lipoapoptosis by inhibiting the RAC1-mediated JNK activation and lipoapoptosis signaling pathway. 

Objective To evaluate whether the plasma CD100 (pCD100) concentration could predict the clinical outcome of patients with nasopharyngeal carcinoma (NPC). Methods A total of 60 patients and 23 healthy doners were enrolled. Their plasma concentrations of CD100 were measured by ELISA, and EBV DNA loads were detected by real-time PCR. The relationship between pCD100 concentrations and outcomes of NPC patients was analyzed. Results The pCD100 concentrations were higher in NPC patients than in health controls (P < 0. 0001). In addition, the pCD100 concentrations were significantly elevated in NPC patients with recurrence or metastasis than those without recurrent and metastasis (P< 0. 0001). Cox analysis showed that the concentration of pCD100 was associated with 5-year progression-free survival ( PFS) rate in NPC patients ( P < 0. 0001), and was an independent prognostic factor for PFS of NPC patients. Conclusion The pCD100 concentration is associated with NPC recurrence or metastasis and could be a potential noninvasive prognostic marker for NPC.

Objective To explore the expression and clinical significance of cellular inhibitor of apoptosis protein 2 (c-IAP2) in nasopharyngeal carcinoma (NPC). Methods The NPC tissues and the nasopharyngeal normal tissues were obtained from 95 NPC patients and 40 non-NPC patients, respectively, and their clinico-prognostical data were analyzed. The expression of c-IAP2 mRNA and protein in these tissues was detected by RT-PCR, immunochemistry and Western blotting, respectively. The relationship between the clinicopathological characteristics and c-IAP2 expression was analyzed by the chi-square test. Kaplan-Meier combined with Log-rank was used to test the survival difference of patients with different expression levels of c-IAP2. Moreover, univariate and multivariate Cox proportional risk regression models were used to analyze the risk factors affecting the prognosis of NPC patients. Results RT-PCR showed that the mRNA expression level of cIAP2 was significantly increased in NPC tissues when compared with normal tissues (t =12. 62, P< 0. 001). Western blotting analysis showed that the expression level of c-IAP2 protein was significantly up-regulated in NPC tissues, which was consistent with the change of c-IAP2 mRNA expression level. Furthermore, the immunohistochemical analysis displayed that c-IAP2 was highly expressed in NPC tissues, and its expression level was associated with tumor differentiation, T staging, N staging, and TNM staging (P < 0. 05, respectively). Survival analysis found that the overall survival rate in NPC patients with low c-IAP2 expression level was significantly higher than that in NPC patients with high c-IAP2 expression level (χ 2 = 11. 86, P = 0. 001), and the high expression of cIAP2 was an independent risk factor for shortened overall survival of patients with NPC ( HR = 2. 425, 95% CI: 1. 256 ~ 4. 994, P = 0. 012). Conclusion The expression level of c-IAP2 in NPC is significantly up-regulated, and its high expression is significantly correlated with the poor prognosis of NPC patients, which has potential clinical value for evaluating the prognosis of patients with NPC.

Objective To investigate the expression and mechanism of miR-183-5p in zebrafish (Danio rerio) ZF4 cells during low temperature acclimatization. Methods ZF4 cells were cultured under 18℃ for 30 days. The expression of miR-183-5p in ZF4 cells was detected by RT-qPCR. Cell viability was determined by CCK-8 cell viability assay after transfection of miR-183-5p mimics/ miRNC with Turbofect cell transfection kit. Targetscan Fish database was used to predict the potential target genes, and dual luciferase activity reporting assay was used to confirm the binding site of miR-183-5p and its target gene egr1. Results The expression level of miR-183-5p increased significantly. The conservation analysis showed that miR-183-5p was highly conserved among species. Overexpression of miR-183-5p could enhance the viability of ZF4 cells under low temperature. The potential target genes of miR-183-5p were predicted by bioinformatics methods and tentatively verified by RT-qPCR. The dual luciferase activity reporting assay further confirmed that miR-183-5p could bind to the 3′UTR of egr1. Conclusion This study demonstrates that miR-183-5p plays a protective role in ZF4 cells during low temperature acclimatization through egr1 in zebrafish. It lays a foundation for further exploration of the mechanisms of zebrafish during low temperature acclimation and provides a new idea for the researches of molecular mechanisms of hypothermia treatment.

Objective To explore the alleviating effect of calcium / calmodulin-dependent protein kinase kinase β ( CaMKKβ) overexpression on high-fat induced non-alcoholic liver disease (NAFLD). Methods The SD rats were enrolled and divided into Control group, NAFLD group, NAFLD + LV group and NAFLD + LV-CaMKKβ group. The high-fat diet was applied to establish the NAFLD mouse models. Mice in the NAFLD + LV group and NAFLD + LV-CaMKKβ group were injected with lentivirus with empty vector and lentivirus with CaMKKβ-overexpression vector through the tail vein, respectively. The expression of CaMKKβ protein in liver tissues, the fatty vacuoles, the pathological tissues, the liver function indexes, the lipid accumulation, the oxidative damage markers, the AMPKα1 and Nrf2 phosphorylation and the positive expression of NF-κB P65 were detected and compared among the four groups. Results CaMKKβ overexpression led to a sharp contrast between the nucleus and cytoplasm in liver cells. The number of necrotic cells was significantly reduced. The lipid accumulation was significantly improved. The phosphorylations of Nrf2 and AMPKα1 in liver tissues were increased. The level of serum SOD was significantly increased (P < 0. 05). The levels of serum ALT, AST, TC, TG, MDA and LDH were significantly decreased, and the positive rate of NF-κB P65 cells was profoundly decreased as well (P< 0. 05). Conclusion Overexpression of CaMKKβ can alleviate high-fat induced NAFLD, which may be through inhibiting oxidative and inflammation response.

Objective To explore the expression of miR-188-3p in hepatocellular carcinoma (HCC ) and its molecular mechanism of inhibiting the invasion and migration of HCC cells. Methods The expression of miR-188-3p in human HCC tissues and cell lines was detected by RT-qPCR, and the clinical value of miR-188-3p expression in HCC was further analyzed. Western blotting was used to detect the effects of transfection of the miR-188-3p mimics and inhibitor on YAP1 protein in HCC cells. Transwell invasion and migration assay were used to measure the invasive and migratory abilities of cells in each group, respectively. Dual luciferase gene reporting assay was employed to identify the mechanism of miR-188-3p targeting YAP1. Finally, the recovery experiment was performed by co-transfection of miR-188-3p mimics and YAP1 overexpression plasmid in HCC cells. Results The expression level of miR-188-3p was significantly lower in HCC tissues than that in normal liver tissues, and its low expression was closely related to tumor size, tumor differentiation, and TNM stage ( P < 0. 05, respectively). Further survival analysis showed that low miR-188-3p expression level in HCC tissues suggested a poor prognosis (log-rankP = 0. 025). In vitro cell experiments showed that the overexpression of miR-188-3p significantly inhibited the invasion and migration of HCC cells, while inhibition of miR-188-3p expression showed an opposite effect. Dual luciferase reporter gene assay showed that miR-188-3p could inhibit the expression of YAP1 protein by binding to the 3′UTR of YAP1. The results of the recovery experiment confirmed that miR-188-3p inhibited the invasion and migration of HCC cells by inhibiting the expression of YAP1 protein. Conclusion The expression of miR-188-3p is down-regulated in HCC, and miR-188-3p inhibits the invasion and migration of HCC cells by targeting the expression of YAP1, thereby participating in the occurrence and progression of HCC.

Objective To explore the effects of miR-4792 on the proliferation, migration and invasion of pancreatic cancer. Methods GSE59856 and GSE71533 data sets were downloaded. The intersection of the up-regulated genes in the two data sets was the gene miR-4792. Pancreatic cancer cell lines PANC-1 and SW1990, which could overexpress miR-4792, were then constructed. The cell proliferation was measured by CCK-8. Cell migration and invasion were measured by transwell chamber assay. The effects of miR-4792 overexpression on tumor growth were determined by the subcutaneous xenograft model of nude mice. The target genes of miR-4792 were predicted by Targetscan. GSE62452 and TCGA data sets were downloaded to screen out the gene beta-site APP cleaving enzyme-1 (BACE1). The relationship between the BACE1 expression and the clinical phenotypes of malignant pancreatic cancer was analyzed. The relationship between miR-4792 and its target BACE1 was verified. Results In the miR-4792 group relative to the miR-NC group, the miR-4792 level, the cell proliferation ability and the number of migratory and invasive cells were significantly increased. The tumor volume was significantly enhanced in miR-4792 group compared with miR-NC group. The volume and weight of the tumor, and the miR-4792 expression level were significantly increased in the miR-4792 group (P< 0. 05). It was predicted by Targetscan that the target gene of miR-4792 was BACE1, whose expression was closely related to the recurrence, proliferation, progression-free survival, prognosis, M staging and G staging of pancreatic cancer (P< 0. 05). It was confirmed by dual luciferase reporter gene assay that miR-4792 could directly act on the 3′UTR of BACE1 to down-regulate its expression. Compared with the miR-NC group, the expression levels of BACE1 mRNA and protein were decreased in the miR-4792 group (P< 0. 05). The expression level of BACE1 protein was significantly increased, and the cell proliferation ability and the number of migration and invasion cells were significantly decreased in the miR-4792 + BACE1 group compared with the miR-4792 group (P < 0. 05). However, the differences of the above indexes between the miR-4792 + BACE1 group and the miR-NC group were not statistically significant ( P > 0. 05). Conclusion The expression of miR-4792 is up-regulated in pancreatic cancer, and its overexpression can promote the proliferation, migration and invasion of pancreatic cancer cells, which may be through the down-regulation of its target gene BACE1.

Objective To investigate the relationship between the activation of complement C5a / C5aR pathway and tumor hypercoagulability and the underlying mechanism in renal carcinoma bearing mice. Methods The cancer and paracancerous tissues of 32 patients with renal cell carcinoma diagnosed by pathological biopsy in the Tangshan People’s Hospital from July 2016 to October 2019 were obtained. The expression levels of C5a / C5aR pathway activation related proteins in tissues were detected by Western blotting. The human ACHN renal cancer cells were inoculated subcutaneously in the axillary region of the BALB / c-nu / nu nude mice. After successful inoculation, they were randomly divided into intervention group and model group, in which the intervention group was injected with C5aR antagonist (C5aRA) via the tail vein, and the model group was injected with normal saline in equal volume, and 6 mice with no subcutaneous inoculation and no C5aRA treatment were taken as the control group. The tumor growth was observed and the levels of hypercoagula bility related indexes were measured. The mice were sacrificed to collect cancer tissues, and the expression levels of C5a / C5aR pathway activation related proteins were detected by Western blotting. Results The tumor volume of mice in the two groups was statistically significant in 6 ~ 21 day, and the tumor volume of the intervention group was significantly lower than that of the model group (P< 0. 05). There was no significant difference in serum D-D, vWF and TF levels in the first day of tumor-bearing mice in the three groups. The serum coagulation index levels in the intervention group and the model group were significantly increased at the 14th day and the 21st day. Moreover, the serum coagulation index levels in the intervention group were significantly lower than those in the model group (P< 0. 05). The expression levels of C5aR, C5b-9, FGL2, P38 and p-P38 in mice cancer tissues in the intervention group were significantly lower than those in the model group ( P < 0. 05). The expression levels of C5aR, C5 b-9, FGL2, P38 and p-P38 in renal carcinoma were significantly higher than those in adjacent tissues (P< 0. 05). There were 14 cases of hypercoagulability and 18 cases of non-hypercoagulability in 32 cases of renal carcinoma. The expression levels of C5aR, C5 b-9, FGL2, P38 and p-P38 in hypercoagulable group were significantly higher than those in non-hypercoagulable group (P< 0. 05). Conclusion Complement C5a / C5aR pathway can induce hypercoagulability of renal carcinoma by regulating the expression of FGL2, and then participate in the pathogenesis of renal carcinoma.

Objective To explore the correlation of the expression of Toll-like receptor-associated molecules (TRAM), Toll-like receptor 4 ( TLR4) and interferon regulatory factor-3 ( IRF3) in peripheral blood mononuclear cells (PBMCs) with the plaque stability and National Institutes of Health Stroke Scale (NIHSS) scores in patients with acute cerebral infarction (ACI). The predictive value of these clinical indicators for the prognosis of ACI was also investigated. Methods A total of 115 patients with ACI were recruited from the Affiliated Hospital of Yan’an University during January 2018 to September 2020. All of them received intravenous thrombolysis and were followed up for 90 days. They were divided into two groups according to the modified Rankin score (mRS): good prognosis group (78 cases) and poor prognosis group (37 cases). The clinical data were analyzed and the mRNA expression levels of TRAM, TLR4 and IRF-3 in PBMCs were compared between the two groups. The correlation of clinical indicators in PBMCs between the two groups and their relationship with plaque stability and NIHSS score were evaluated. COX regression analysis was used to analyze the relationship between TRAM, TLR4, IRF-3 mRNA expression levels in PBMC and the poor prognosis. Receiver operating characteristic (ROC) curve was used to evaluate the predictive value of each index in PBMCs for the prognosis of ACI. Results There were statistically significant differences in the time from onset to thrombolysis, the plaque stability, the NIHSS score, and the diabetes ratio between the two groups (P < 0. 05). The mRNA expression levels of TRAM, TLR4 and IRF-3 in PBMCs in the poor prognosis group were higher than that in the good prognosis group (P< 0. 05). Pearson correlation analysis showed that the mRNA expression levels of TRAM, TLR4 and IRF-3 in PBMCs were positively correlated with the NIHSS score (P < 0. 05). Spearman correlation analysis showed that the mRNA expression levels of TRAM, TLR4 and IRF-3 were negatively correlated with the plaque stability (P< 0. 05). COX regression analysis showed that the mRNA expression levels of TRAM, TLR4 and IRF-3 in PBMCs were significantly correlated with poor prognosis after adjusting for the confounding factors including time from onset to thrombolysis, plaque stability, NIHSS score and diabetes (P < 0. 05). In ROC curve analysis, the mRNA expression levels of TRAM, TLR4 and IRF-3 were fitted with Logistic binary regression, and the return prediction probability Logit ( P) was used as an independent test variable. The combined prediction AUC obtained was 0. 886 (95 % CI 0. 824 ~ 0. 948, P < 0. 001). The sensitivity of the prediction was 83. 78 % , and the specificity was 78. 21 % , which were better than those in single prediction of each index. Conclusion The mRNA expression levels of TRAM, TLR4 and IRF-3 in PBMC are significantly correlated with plaque stability and NIHSS score of ACI patients. Combined detection method has a reliable value in predicting poor prognosis for ACI patients. 

Objective To explore the protective effect of coumarin glycosides on podocyte injury by regulating phosphoinositide 3-kinase (PI3K) -protein kinase B (AKT) -mammalian target of rapamycin (mTOR) signaling pathway in rats with diabetic nephropathy. Methods The rat model of diabetic nephropathy was constructed by intraperitoneal injection of streptozotocin ( STZ), and different doses of coumarin glycosides extracted from hydrangea paniculata ( HP), were used to treat the rat model of diabetic nephropathy. Blood glucose, urine protein and endogenous creatinine clearance rate in rats were measured. Immunohistochemistry (IHC) was applied to detect the apoptosis of podocytes in rats. Real-time fluorescent quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) was used to detect the mRNA expression levels of podocyte split membrane proteins Nephrin, Prodocin, and Desmin, a podocyte injury marker. Western blotting was adopted to detect the expression levels of proteins in PI3K/ AKT / mTOR signaling pathway and their phosphorylation. Results HP could significantly improve the renal function in the rat model. In the model group relative to the control group, the expression levels of fibronectin and type Ⅳ collagen were significantly increased, and the expression levels of Nephrin and Prodocin were significantly downregulated while the expression of Desmin was significantly up-regulated, and the phosphorylation level of PI3K/ AKT / mTOR was decreased significantly (P < 0. 05). With the dose of HP treatment increased, the expression levels of fibronectin and type Ⅳ collagen were decreased, and the expression levels of Nephrin and Prodocin were up-regulated while the expression of Desmin was downregulated in a HP dose-dependent manner, and the PI3K/ AKT / mTOR signaling pathways were significantly activated (P< 0. 05) when compared to the model group. Conclusion Coumarin glycosides can reduce the podocyte injury in rats with diabetic nephropathy by activating the PI3K/ AKT / mTOR signaling pathway.

Objective To explore the mechanism by which the glucagon-like peptide-1 receptor (GLP-1R) agonist ( exendin-4 ) reduces the inflammation and endothelial damage induced by high glucose in macrophages. Methods Mouse monocyte macrophage leukemia cells (RAW264. 7) were divided into groups as follows: control group (RAW264. 7 cells cultured in normal medium) ; high glucose induction group (RAW264. 7 cells cultured in high glucose medium) ; exendin-4 group ( RAW264. 7 cells cultured in high glucose medium supplemented with exendin-4). The mRNA expression level of GLP-1R was detected by RT-qPCR. The mRNA expression levels of M1 pro-inflammatory factors nitric oxide synthase ( iNOS) , interleukin ( IL) -6, tumor necrosis factor ( TNF) -α ( TNF-α) and M2 specific gene IL-10, mannose receptor 1 (MRC-1) , macrophage galectin 1 ( MGL-1) , arginine-1 ( ARG-1) were also detected by RTqPCR. The expression levels of VE-cadherin, ZO-1, intercellular adhesion molecule-1 ( ICAM1) and vascular cell adhesion molecule-1 (VCAM-1) were detected by Western blotting. The expression levels of p-STAT3 and p-JNK were analyzed by Western blotting. Results  The expression level of GLP-1R mRNA was significantly decreased in the high glucose induced group compared with the control group ( P < 0. 05). The expression level of GLP-1R mRNA was significantly increased (P < 0. 05) in the exendin-4 group compared with the high glucose induction group. In the high glucose induced group relative to the control group, the expression levels of iNOS, IL-6 and TNF-α mRNA were significantly increased, and the expression levels of IL-10, MRC-1, MGL-1 and ARG-1 mRNA were significantly decreased (P < 0. 05). These indicators were significantly improved in the exendin-4 group compared with the high glucose induced group (P < 0. 05) . Compared with the control group, the expression levels of VE-cadherin and ZO-1 in the high glucose induced group were decreased, and the expression levels of ICAM-1 and VCAM-1 were increased (P < 0. 05 ) , which were significantly reversed in the exendin-4 group ( P < 0. 05 ) . Compared with the control group, the protein expression levels of p-STAT3 and p-JNK in the high glucose induced group were increased ( P < 0. 05). They were significantly decreased in the exendin-4 group when compared with the high glucose induced group (P < 0. 05). Conclusion Exendin-4 can inhibit the activation of the JNK-STAT3 pathway, promote M2 polarization and inhibit M1 polarization, reduce the expression of ICAM-1 and VCAM-1, and alleviate high glucose-induced macrophage inflammatory response.

Objective To investigate whether long intergenic non-coding RNA 00659 (LINC00659) targets miR-149-5p to regulate the proliferation, migration, invasion and radiosensitivity of esophageal squamous cell carcinoma Eca-109 cells. Methods The expression of LINC00659 and miR-149-5p in 30 pairs of esophageal squamous cell carcinoma tissues and control tissues was analyzed using real-time quantitative PCR (RT-qPCR). Eca-109 cells cultured in vitro were divided into si-NC group, si-LINC00659 group, miR-NC group, miR-149-5p group, siLINC00659 + anti-miR-NC group, and si-LINC00659 + anti-miR-149-5p group. The effects of LINC00659 and miR-149-5p on the proliferation of Eca-109 cells were measured by CCK-8 cell viability assay. The effects of LINC00659 and miR-149-5p on the migration and invasion of Eca-109 cells were determined through Transwell migration / invasion assay. The colony formation test was used to measure the survival fraction and radiosensitization ratio of Eca-109 cells. The relationship between LINC00659 and miR-149-5p was verified by dual luciferase report experiment. Results The expression level of LINC00659 was significantly higher in the esophageal squamous cell carcinoma tissue than in the control group, while the expression level of miR-149-5p was significantly lower in the esophageal squamous cell carcinoma tissue than in control tissues (P< 0. 05). Compared with the si-NC group, the proliferation inhibition rate of Eca-109 cells in the si-LINC00659 group was increased, and the number of migratory / invasive cells and the cell survival fraction were decreased (P< 0. 05). The radiosensitization ratio of Eca-109 cells in the si-LINC00659 group was 1. 938. In the miR-149-5p group relative to the miR-NC group, the proliferation inhibition rate of Eca-109 cells was increased, and the number of migratory / invasive cells and the cell survival fraction were decreased (P< 0. 05). The radiosensitization ratio of Eca-109 cells in the miR-149-5p group was 1. 545. miR-149-5p was the target gene of LINC00659. Compared with the si-LINC00659 + anti-miRNC group, the proliferation inhibition rate of Eca-109 cells in si-LINC00659 + anti-miR-149-5p group was decreased, and the number of migratory / invasive cells and the cell survival fraction were increased (P < 0. 05). The radiosensitization ratio of Eca-109 cells in si-LINC00659 + anti-miR149-5p group was 0. 657. Conclusion The interference of LINC00659 inhibits cell proliferation, migration and invasion, improves cell radiosensitivity of esophageal squamous cell carcinoma Eca109 cells by up-regulating miR-149-5p.

Objective To investigate the effect of long-chain noncoding RNA small nucleolar RNA host gene 11 ( SNHG11) on the proliferation of colorectal cancer and its molecular mechanism. Methods SNHG11 overexpression or knock-down cell lines were constructed in human colon cancer cell lines LoVo and SW480. The proliferation ability of the colorectal cancer cells was assayed after SNHG11 overexpression or knock-down. The expression levels of P50, P65 and NF-κB downstream signaling proteins were detected after overexpression and interference of SNHG11 in colorectal cancer cell lines. Results Overexpression of SNHG11 could promote the proliferation of colorectal cancer cells, while inhibition of SNHG11 expression could significantly inhibit the proliferation of colorectal cancer cells. The expression levels of P65, P50, NF-κB downstream signaling proteins and the expression levels of proliferation-related genes c-myc, COX2, CCND1 and VEGFA were significantly up-regulated after overexpression of SNHG11. However, their expression levels were decreased significantly after knock-out of SNHG11. SNHG11 could up-regulate NF-κB complex and activate NFκB signaling pathway via binding to P50 in the NF-κB complex. Conclusion Long non-coding RNA SNHG11 promotes colorectal cancer cell proliferation by activating NF-κB signaling pathway. 

Peroxisome proliferator activated receptors ( PPARs), which includes PPARα, PPARδ and PPARγ, belong to the superfamily of nuclear hormone receptors. The expression of the three isoforms of PPARs in different tissues showed distinct specificities. PPARγ is present in the adipose tissue, heart, intestine, and immunocytes. It exerts important function in adipogenesis. PPARγ is found to have the antioxidant activity, which may be through the Nrf2 signaling pathway, endothelial NOS ( eNOS) expression, inducible NOS ( iNOS) expression and some other related signaling pathways. Radiation-induced oxidative stress is the predominant factor that leads to the damage at both the cellular level and systemic level. As PPARγ acts to protect from oxidative stress, it may serve as an effective radioprotective and radiotherapeutic target.