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 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 To study the drug resistance genes in imipenem-resistant Pseudomonas aeruginosa.METHODS Five main drug resistance genes:IMP,VIM,SPM and GIM which are pertinent with metal ?-lactamase and outer membrane protein oprD2 gene were analyzed using PCR method.RESULTS The oprD2 genes in 48 strains of imipenem-resistant P.aeruginosa were negative,and in 14 strains were positive from all 62 strains tested.There were 16 strains with positive IMP type and 5 strains with positive VIM type metal enzyme genes positive,7 metal enzymes producing strains were with negative oprD2 gene.The SPM and GIM metal enzyme genes detected were all negative.CONCLUSIONS The loss of outer membrane protein oprD2 gene is the main mechanism of imipenem resistance in P.aeruginosa in Tai′an area.

Objective:To summarize and elucidate the impact of ambient air pollution on biological aging among middle-aged and older adults.Methods:"Air pollution""Biological age""Epigenetic age""Biological aging"and"Epigenetic aging", as well as specific names of air pollutants and biological age were used as search keywords. This study searched the databases of PubMed and Web of Science for eligible English articles and CNKI, CQVIP, Wanfang, CBM, CSTP and other Chinese databases for eligible Chinese articles from inception until June 30, 2023. The language was limited to Chinese and English.Results:Among the 14 included articles, five studies investigated the impact of air pollution on DNA methylation age using different algorithms, while six studies explored the relationship between air pollutants and telomere length. Six studies focused on frailty as an outcome, and an additional study revealed the relationship between fine particulate matter (PM 2.5) and its components with composite indicator age (KDM age). The results indicated that, although different forms of biological ages were susceptible to different ambient air pollutants at different degrees, previous studies had consistently found that the increased levels of PM 2.5 and one of its major components, black carbon (BC), could significantly accelerate the biological aging of middle-aged and older adults. Similar trends were observed with nitrogen oxides (NO x) and ozone (O 3) but with relatively limited evidence. Conclusion:Major air pollutants could accelerate the biological aging of middle-aged and older adults.

Objective:To summarize and elucidate the impact of ambient air pollution on biological aging among middle-aged and older adults.Methods:"Air pollution""Biological age""Epigenetic age""Biological aging"and"Epigenetic aging", as well as specific names of air pollutants and biological age were used as search keywords. This study searched the databases of PubMed and Web of Science for eligible English articles and CNKI, CQVIP, Wanfang, CBM, CSTP and other Chinese databases for eligible Chinese articles from inception until June 30, 2023. The language was limited to Chinese and English.Results:Among the 14 included articles, five studies investigated the impact of air pollution on DNA methylation age using different algorithms, while six studies explored the relationship between air pollutants and telomere length. Six studies focused on frailty as an outcome, and an additional study revealed the relationship between fine particulate matter (PM 2.5) and its components with composite indicator age (KDM age). The results indicated that, although different forms of biological ages were susceptible to different ambient air pollutants at different degrees, previous studies had consistently found that the increased levels of PM 2.5 and one of its major components, black carbon (BC), could significantly accelerate the biological aging of middle-aged and older adults. Similar trends were observed with nitrogen oxides (NO x) and ozone (O 3) but with relatively limited evidence. Conclusion:Major air pollutants could accelerate the biological aging of middle-aged and older adults.