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Objective:To explore the anti-aging effects of berberine hydrochloride and underlying mechanism.Methods:Twelve 4-week-old C57BL6/J mice were divided into aging group (fed with normal chaw), aging+ BBR intervention group(fed with normal chaw containing 1 g/kg berberine hydrochloride). At the age of 64 weeks, all the experimental mice were executed. The liver tissues were made into paraffin sections for HE staining to observe the morphological and structural integrity of liver parenchymal cells for pathological evaluation. Immunofluorescence was used to detect p16 protein expression levels in liver. The expression levels of malondialdehyde(MDA), superoxide dismutase(SOD), and glutathione peroxidase(GSH-Px) were detected by colorimetry. The expression levels of interleukin(IL)-1β, IL-6, and tumor necrosis factor-α(TNF-α) in liver tissues and IL-8 in serum were detected by enzyme linked immunosorbent assay(ELISA) technique. The p16, p21, nuclear factor erythroid-2 related factor 2(Nrf2), nuclear factor-κB(NF-κB), phospho(p-)NF-κB, inhibitory κB(IκB)α, p-IκBα, and p38 mitogen-activated protein kinase(MAPK) protein expression levels in liver were detected by Western blotting. The same indices were tested in the 16-week-old mice as the young control group.Results:Compared with the young control group, the liver tissue in the aging control group exhibited morphological aging and antioxidant capacity were reduced( P<0.01), and inflammatory factors were increased( P<0.05 or P<0.01). Compared with the aging group, the liver tissues in the aging+ BBR intervention group were still maintain regular arrangement of hepatocytes, the p16 and p21 protein expression levels were significantly increased( P<0.05 or P<0.01), the antioxidant capacity were increased( P<0.05 or P<0.01), the level of inflammatory factors were decresed( P<0.05 or P<0.01), and the p38 MAPK/NF-κB pathway and Nrf2 pathway were inhibited( P<0.001). Conclusion:Berberine hydrochloride improves the aging morphology of the liver, potentially by suppressing the p38 MAPK/NF-κB pathway to reduce inflammation levels and inhibiting the Nrf2 pathway to ameliorate oxidative stress.
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BackgroundSkeletal muscle is the largest tissue in the human body, and it plays a major role in exerting force and maintaining metabolism homeostasis. The role of muscle transcription factors in the regulation of metabolism is not fully understood. MondoA is a glucose-sensing transcription factor that is highly expressed in skeletal muscle. Previous studies suggest that MondoA can influence systemic metabolism homeostasis. However, the function of MondoA in the skeletal muscle remains unclear.MethodsWe generated muscle-specific MondoA knockout (MAKO) mice and analyzed the skeletal muscle morphology and glycogen content. Along with skeletal muscle from MAKO mice, C2C12 myocytes transfected with small interfering RNA against MondoA were also used to investigate the role and potential mechanism of MondoA in the development and glycogen metabolism of skeletal muscle.ResultsMAKO caused muscle fiber atrophy, reduced the proportion of type II fibers compared to type I fibers, and increased the muscle glycogen level. MondoA knockdown inhibited myoblast proliferation, migration, and differentiation by inhibiting the phosphatase and tensin homolog (PTEN)/phosphoinositide 3-kinase (PI3K)/Akt pathway. Further mechanistic experiments revealed that the increased muscle glycogen in MAKO mice was caused by thioredoxin-interacting protein (TXNIP) downregulation, which led to upregulation of glucose transporter 4 (GLUT4), potentially increasing glucose uptake.ConclusionMondoA appears to mediate mouse myofiber development, and MondoA decreases the muscle glycogen level. The findings indicate the potential function of MondoA in skeletal muscle, linking the glucose-related transcription factor to myogenesis and skeletal myofiber glycogen metabolism.
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BackgroundSkeletal muscle is the largest tissue in the human body, and it plays a major role in exerting force and maintaining metabolism homeostasis. The role of muscle transcription factors in the regulation of metabolism is not fully understood. MondoA is a glucose-sensing transcription factor that is highly expressed in skeletal muscle. Previous studies suggest that MondoA can influence systemic metabolism homeostasis. However, the function of MondoA in the skeletal muscle remains unclear.MethodsWe generated muscle-specific MondoA knockout (MAKO) mice and analyzed the skeletal muscle morphology and glycogen content. Along with skeletal muscle from MAKO mice, C2C12 myocytes transfected with small interfering RNA against MondoA were also used to investigate the role and potential mechanism of MondoA in the development and glycogen metabolism of skeletal muscle.ResultsMAKO caused muscle fiber atrophy, reduced the proportion of type II fibers compared to type I fibers, and increased the muscle glycogen level. MondoA knockdown inhibited myoblast proliferation, migration, and differentiation by inhibiting the phosphatase and tensin homolog (PTEN)/phosphoinositide 3-kinase (PI3K)/Akt pathway. Further mechanistic experiments revealed that the increased muscle glycogen in MAKO mice was caused by thioredoxin-interacting protein (TXNIP) downregulation, which led to upregulation of glucose transporter 4 (GLUT4), potentially increasing glucose uptake.ConclusionMondoA appears to mediate mouse myofiber development, and MondoA decreases the muscle glycogen level. The findings indicate the potential function of MondoA in skeletal muscle, linking the glucose-related transcription factor to myogenesis and skeletal myofiber glycogen metabolism.
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【Objective】 To investigate and analyze the current situation of the human resources as well as blood collection and supply of blood banks of Zhejiang Province, so as to understand the problems existing in the development of human resources and put forward suggestions. 【Methods】 Questionnaires were issued to Blood Center of Zhejiang Province, municipal central blood stations, and county-level central blood banks to investigate the relevant data in 2015 and 2019. Meanwhile, some data were obtained through the Zhejiang Blood Management Information System (BIS3.0), symposiums, and querying medical service data. Statistical analysis was carried out. 【Results】 Among the 28 blood banks, filled the questionnaires, 927 personnel were in accordance with the authorized strength, accounting for 62.26% (927/1 489), and 1069 health technicians, accounting for 71.519% (1 060/1 489). From 2015 to 2019, the annual growth rate of human resources in blood banks was 2.02%, lower than the annual growth rate of whole blood collection volume 4.83% and the annual growth rate of clinical blood supply (red blood cell) 4.82%, lagging behind the annual growth rate of 6.55%, 8.71% and 12.36% in the number of diagnoses, inpatients and surgeries in the hospitals across the province. The average annual growth rate of doctors and nurses in blood banks was 0.17% and 1.67%, lower than that of licebsed doctors and registered nurses of the province, which was 6.78% and 8.27%, respectively. 【Conclusion】 With the development trend of blood collection and supply, the personnel allocation and the proportion of health technicians of blood banks across Zhejiang Province is insufficient. It is suggested to establish a manpower allocation standard suitable to the business volume, give priority to properly solvement of the current employment, strengthen training, and improve the efficiency of physical examination consultation, testing and phlebotomy positions.
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Objective@#To study the effects of resistant dextrin (RD) on liver fat deposition in high-fat diet-fed (HFD) mice, and to further explore whether it can regulate the AMPK signaling pathway.@*Methods@#Thirty-six 4-week-old male C57BL/6 mice were randomly divided into three groups: normal control group (chow), high-fat diet group (HFD), and high-fat diet+ resistant dextrin group (HFD+ RD, 10 g·kg-1·d-1). After 12 weeks of intervention, the liver tissues and serum samples were collected. Serum triglyceride (TG), total cholesterol (TC), low-density lipoprotein-cholesterol (LDL-C), high-density lipoprotein-cholesterol (HDL-C), aspartate aminotransferase (AST), alanine transaminase (ALT) levels and liver TG were measured. Liver tissue HE and oil red O staining were performed to observe hepatocyte steatosis and liver fat deposition. Quantitative real-time PCR was performed to detect the relative expression of fatty acid synthesis related genes SREBP1, ACC, SCD1 in the liver tissue, and Western blot was performed to detect relative protein levels of pAMPK, SREBP1, Fasn, and ACC in the liver.@*Results@#Compared with chow group, the body weight gain, fasting blood glucose (FBG), serum TC, LDL-C, HDL-C, and ALT levels were increased in HFD group (P<0.01), and serum AST level was also increased (P<0.05). Moreover, liver oil red O staining revealed that liver fat deposition was much more obvious in HFD group than that in chow group, and liver TG was also increased in HFD group (P<0.01). The mRNA levels of SREBP1 and ACC were increased in HFD group compared with that in chow group, and the protein level of pAMPK was reduced in HFD group (P<0.05). As compared with HFD group, the body weight gain, serum TG, TC, LDL-C, HDL-C and ALT levels were significantly reduced in RD group (P<0.01), and FBG level was also reduced (P<0.05). Moreover, RD treatment alleviated liver fat deposition and TG accumulation (P<0.01). The mRNA levels of SREBP1, ACC, and SCD1 were all reduced in RD group compared with HFD group. The protein level of pAMPK was increased, and the expression of Fasn was reduced with RD treatment (P<0.01).@*Conclusion@#Resistant dextrin improves liver fat deposition and activates the AMPK signaling pathway in HFD-fed mice.
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Objective:To study the effects of resistant dextrin (RD) on liver fat deposition in high-fat diet-fed (HFD) mice, and to further explore whether it can regulate the AMPK signaling pathway.Methods:Thirty-six 4-week-old male C57BL/6 mice were randomly divided into three groups: normal control group (chow), high-fat diet group (HFD), and high-fat diet+ resistant dextrin group (HFD+ RD, 10 g·kg -1·d -1). After 12 weeks of intervention, the liver tissues and serum samples were collected. Serum triglyceride (TG), total cholesterol (TC), low-density lipoprotein-cholesterol (LDL-C), high-density lipoprotein-cholesterol (HDL-C), aspartate aminotransferase (AST), alanine transaminase (ALT) levels and liver TG were measured. Liver tissue HE and oil red O staining were performed to observe hepatocyte steatosis and liver fat deposition. Quantitative real-time PCR was performed to detect the relative expression of fatty acid synthesis related genes SREBP1, ACC, SCD1 in the liver tissue, and Western blot was performed to detect relative protein levels of pAMPK, SREBP1, Fasn, and ACC in the liver. Results:Compared with chow group, the body weight gain, fasting blood glucose (FBG), serum TC, LDL-C, HDL-C, and ALT levels were increased in HFD group ( P<0.01), and serum AST level was also increased ( P<0.05). Moreover, liver oil red O staining revealed that liver fat deposition was much more obvious in HFD group than that in chow group, and liver TG was also increased in HFD group ( P<0.01). The mRNA levels of SREBP1 and ACC were increased in HFD group compared with that in chow group, and the protein level of pAMPK was reduced in HFD group ( P<0.05). As compared with HFD group, the body weight gain, serum TG, TC, LDL-C, HDL-C and ALT levels were significantly reduced in RD group ( P<0.01), and FBG level was also reduced ( P<0.05). Moreover, RD treatment alleviated liver fat deposition and TG accumulation ( P<0.01). The mRNA levels of SREBP1, ACC, and SCD1 were all reduced in RD group compared with HFD group. The protein level of pAMPK was increased, and the expression of Fasn was reduced with RD treatment ( P<0.01). Conclusion:Resistant dextrin improves liver fat deposition and activates the AMPK signaling pathway in HFD-fed mice.
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Objective To compare with the characteristics of different demographic and blood donation behaviors of the first blood donors and the repeated blood donors,to analyze the related factors influencing the repeated blood donation behavior,to provide the evidence to develop the recall strategy for the retention of the first-time donors strategies.Methods Use methods such as the composition ratio of descriptive analysis,and logistic regression analysis,Retrospectively analyzed the data of 3 226 571 cases of the whole blood donors in Zhejiang province from 2006 to 2015.from BIS2.0 Results ZheJiang repeated blood donors in 2006-2015 is accounted for 30.8%,men (57.8%),the proportion of aged 25 above is higher than the first blood donors;71.7% of men in the repeated blood donors are 60-79 kg,52.2% of women repeated blood donors are 50 to 59 kg;40% of the repeat donors blood for the first time donate 400 mL;71.6% of the repeated blood donors to donate again in 0.5-2 years,and of these,40.8% back in 0.5-1 year.Conclusion The main factors on the demographic aspects that influence the repeated blood donation is occupation,cultural degree,the quantity of blood donation for the first time.The characteristics of the precise recall people are as follows:Age 26 to 45 years old,stable career,donate 400 mL for the first-time,weight 70-89 kg of male,weight 55 kg above of women.The better recall intervention Interval is preferred to 0.5-2 years,and 0.5-1 year is the best.