Objective The aim of this study was to investigate the effects of hesperidin ( HDN) on antioxidant ac-tivity in mice.Methods HDN scavenging free radicals was detected by spectrophotometry, inhibition of mitochondrial swelling was detected by pyrogallol autoxidation, and erythrocyte hemolysis was detected by Fe2+phenanthroline.The mice were fed with HDN at different concentrations (0, 80, 160, 320 mg/kg) by gastric gavage for 12 days.ELISA and spec-trophotometric methods were used to assay the amount of MDA in mouse liver and kidney tissues and the activity of antioxi-dant enzymes ( SOD, CAT, GSH-PX) , and the antioxidant enzyme gene mRNA expression was analyzed by RT-PCR.Re-sults Compared with the control group, the radical (· OH, O2 -· , DPPH· ) clearance rate was significantly increased in the HDN groups.There was a significant decrease of oxidative hemolysis of erythrocytes and mitochondrial swelling in vitro. MDA content in the mouse liver and kidney tissues and serum showed a decrease, and the activity of antioxidant enzymes ( SOD, CAT, GSH-PX) in the HDN group was significantly higher than that in the control group.There was an up-regula-tion of mRNA expression of antioxidant enzyme in mouse liver and kidney tissues.Conclusions The results showed that HDN can eliminate free radicals, reduce cell oxidative damage caused by free radicals, inhibit superoxide production, up-regulate antioxidant enzyme gene expression and enhance their enzyme activity, thus showing a good antioxidant effect.

Objective The purpose of this study was to investigate the mechanism of action of polypeptide extracts of Eupolyphaga sinensis Walker ( ESW) against oxidative aging.Methods Mice were intraperitoneally injected D-galac-tose for consecutive 20 days to establish an aging mouse model.The model mice were administered with different doses of ESW polypeptide (0, 40, 80, 160 mg/kg/d).The normal activity, movement and anti-stress ability of the mice were ob-served.The activity of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-PX) in blood and different tissues and the content of glutathione ( GSH) and malondialdehyde ( MDA) of the aging mice were assessed by xanthin oxidase activity measurement and spectrophotometry, respectively.The expression of nuclear factor erythroid 2-re-lated factor 2 (Nrf2) in Caco-2 cells was detected by immunofluorescence.Results Comparing the control and polypep-tide groups, there were significant decreases of body weight gain, organ indexes, anti-stress ability and activity capacity, the activity of SOD, CAT, GSH-PX and the content of GSH, and an increase of the content of MDA in blood and different tissues in the aging mice.With the increasing dose of polypeptide extracts of ESW, the body weight gain, organ indexes of the liver, spleen and kidney were significantly increased, the static and dynamic exercise time was prolonged in the poly-peptide group, and their abilities of hypoxia tolerance and heat tolerance were close to that of normal controls.The SOD, CAT, GSH-PX activity and GSH level in blood and different tissues were significantly increased, but MDA content de-creased.The expression of Nrf2 in Caco-2 cell nuclei was significantly increased in the polypeptide group, close to that of the positive control group.Conclusions The results of our study show that polypeptide extracts of ESW improve the anti-stress and antioxidative capacity in D-galactose-induced mouse models of oxidative aging by initiating Nrf2-ARE antioxidant signaling pathway, therefore, delay the oxidative aging in mice.

Objective To analyze the influence of trabecular microstructure modeling on the biomechanical distribution of implant-bone interface with a three-dimensional finite element mandible model of trabecular structure.Methods Dental implants were embeded in the mandibles of a beagle dog.After three months of the implant installation,the mandibles with dental implants were harvested and scaned by micro-CT and cone-beam CT.Two three-dimensional finite element mandible models,trabecular microstructure(precise model) and macrostructure(simplified model),were built.The values of stress and strain of implant-bone interface were calculated using the software of Ansys 14.0.Results Compared with the simplified model,the precise models' average values of the implant bone interface stress increased obviously and its maximum values did not change greatly.The maximum values of quivalent stress of the precise models were 80％ and 110％ of the simplified model and the average values were 170％ and 290％ of simplified model.The maximum and average values of equivalent strain of precise models were obviously decreased,and the maximum values of the equivalent effect strain were 17％ and 26％ of simplified model and the average ones were 21％ and 16％ of simplified model respectively.Stress and strain concentrations at implant-bone interface were obvious in the simplified model.However,the distributions of stress and strain were uniform in the precise model.Conclusions The precise model has significant effect on the distribution of stress and strain at implant-bone interface.

METTL3 and METTL14 are two components that form the core heterodimer of the main RNA m6A methyltransferase complex (MTC) that installs m6A. Surprisingly, depletion of METTL3 or METTL14 displayed distinct effects on stemness maintenance of mouse embryonic stem cell (mESC). While comparable global hypo-methylation in RNA m6A was observed in Mettl3 or Mettl14 knockout mESCs, respectively. Mettl14 knockout led to a globally decreased nascent RNA synthesis, whereas Mettl3 depletion resulted in transcription upregulation, suggesting that METTL14 might possess an m6A-independent role in gene regulation. We found that METTL14 colocalizes with the repressive H3K27me3 modification. Mechanistically, METTL14, but not METTL3, binds H3K27me3 and recruits KDM6B to induce H3K27me3 demethylation independent of METTL3. Depletion of METTL14 thus led to a global increase in H3K27me3 level along with a global gene suppression. The effects of METTL14 on regulation of H3K27me3 is essential for the transition from self-renewal to differentiation of mESCs. This work reveals a regulatory mechanism on heterochromatin by METTL14 in a manner distinct from METTL3 and independently of m6A, and critically impacts transcriptional regulation, stemness maintenance, and differentiation of mESCs.
Animals ; Mice ; Methylation ; Chromatin ; Histones/metabolism* ; RNA, Messenger/genetics* ; Methyltransferases/metabolism* ; RNA/metabolism*