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Objective To study the protective effect and mechanism of maslinic acid (MA) on acute liver injury (ALI) in rats.Methods Fifty BALB/c mice were randomly divided into control group,model group,and low (12.5 mg/kg),medium (25.0 mg/kg) and high doses (50.0 mg/kg) of MA,with 10 rats in each group.The control group was intraperitoneally injected with normal saline.The other groups were intraperitoneally injected with lipopolysaccharide (LPS) (50 mg/kg) and D-Gal N (500 mg/kg) to prepare mouse AL[model.The MA groups were administered with 12.5,25.0,50.0 mg/kg MA 1 h before model establishment,respectively.All the mice were sacrificed 6 h after model establishment,and serum and liver tissues were collected.Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were measured.Hematoxylin-eosin staining was used to observe the pathological changes of liver tissue.Thiobarbituric acid method was used to determine malondialdehyde (MDA).H2O2 reaction product colorimetric was used to determine the content of myeloperoxidase (MPO).The tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) in serum and liver tissue was detected by enzyme-linked immunosorbent assay,respectively.Western Blot was conducted to detect the expression of nuclear factor E2 related factor 2 (Nrf2),heme oxygenase-1 (HO-1) and the activation of nuclear factor-kappa B (NF-κB) pathway.Results Compared with the model group,the liver histopathology in the low,medium and high doses MA groups was significantly improved.The serum ALT and AST levels were decreased,and the differences were statistically significant (all P＜0.05).The contents of MDA and MPO in liver tissues were decreased,and the differences were statistically significant (all P＜0.05).The protein contents of Nrf2 and HO-1 were increased,the differences were statistically significant (all P＜0.05).The NF-κB pathway was inhibited,and the differences were statistically significant (all P＜0.05).The levels of TNF-α and IL-6 in serum and liver tissues were decreased,and the differences were statistically significant (all P＜0.05).Conclusions MA has a protective effect on LPS/D-Gal N-induced ALI,and its mechanism is related to inhibition of NF-κB pathway and activation of Nrf2/HO-1 pathway.
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This study examined the effect of subcellular localization of P21 on the proliferation and apoptosis of HepG2 cells. The coding genes of the wild and the mutant P21 were amplified by mega primer PCR from the plasmid pCEP-WAF1 which contains human P21 cDNA in the nuclear localizational signal (NLS) sequence, and then inserted into the eukaryotic expression vector pDsRed1-C1. The recombinants were transfected into HepG2 cells. The transcription and expression of P21 were determined by RT-PCR and fluorescence microscopy. The cell proliferation was measured by MTT, and the cell cycle and apoptosis of HepG2 cells by flow cytometry. The results of restriction analysis, DNA sequencing and fluorescence microscopy confirmed the construction of the wild and the mutant P21 in the eukaryotic expression plasmid. The plasmid containing the mutant P21 was found to accelerate cell proliferation and the wild P21 plasmid to inhibit cell proliferation. Cell cycle analysis showed that the cell ratio of G(0)/G(1) in the wild type group was significantly increased as compared with that in the mutant type group, and cell apoptosis analysis revealed that the apoptosis rate in the wild type group was much higher than that in the mutant type group. It was concluded that the subcellular localization of P21 may contribute to the development of hepatic cancer.
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Objective To assess ①the effect of signal transducer and activator of transcription (STAT) on pulmonary injury induced by cecal ligation puncture (CLP) in septic rats; ②the biological effect of interleukin (IL)-6 and IL-10 expression in pulmonary injury mediated by STAT in septic rats. Methods Sepsis of rats was induced by CLP. Male Wistar rats were randomly divided into normal control (n=8), CLP group (n=24), and inhibitor (rapamycin, RPM) of STAT pretreatment group (n=24). At serial time points in each group, animals were sacrificed. Then, pulmonary tissue and serum samples were harvested to determine IL-6 and IL-10 mRNA expression by reverse transcription polymerase chain reaction (RT-PCR) and protein expression levels by enzyme-linked immunosorbent assay (ELISA). Meanwhile, pulmonary STAT-1 DNA-binding activity was detected by electrophoretic mobility shift assay (EMSA) . Activity of myeloperoxidase (MPO) as well as histopathology were also evaluated. Results Compared to normal control, pulmonary STAT-1 activity at 6 h, 24 h and 48 h following CLP significantly elevated (P
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[Objective]To compare the results of 3 methods to treat complete dislocation of acromioclavicular joint.[Method]Three different surgical techniques were employed: K-wire tension band(in group A of 26 cases),clavicular hook plate(in group B of 34 cases) and percutaneous screw and K-wire(in group C of 32 cases).There were 78 males and 14 females,and all the cases were acute complete dislocation of acromioclavicular joint.[Result]Eighty-six cases were followed up with an average period of 19 months(13～31 months).Acording to Karlsson's standards,the rate of excellent and good in the three groups was 73.1%,94.1%,93.8% respectively.The mean oprate time was 35.6min,38.6min,28.1 min respectively.The average blood loss was 43.6ml,48.3ml,7.5ml respectively.The average incision length was 8.8cm,8.9cm,0.7cra cm respectively.The complications were 20,9,8 respectively.[Conclusion]Percutaneous coracoclavicular screw and acromioclavicular K-wire fixation has advantages of less opration time and blood loss,cosmetic scar,and a low complication rate,good clinical results.It is believed to be a better method for the treatment of acromioclavicular joint dislocation.
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Objective To investigate the relationship between activation of Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway and multiple organ dysfunction in rats with sepsis. Methods Using a sepsis model produced by cecal ligation and puncture (CLP), 98 male Wistar rats were randomly divided into normal control group (n=10), CLP group (n=40), AG490 (JAK2 inhibitor) treatment group (n=24) and rapamycin (RPM, STAT3 inhibitor) treatment group (n=24). At serial time points, the animals in each group were sacrificed, then tissue samples from the liver, lungs, kidneys and small intestine were harvested to detect STAT1/3 activity, pulmonary myeloperoxidase (MPO) and small intestinal diamine oxidase (DAO) activities. Meanwhile, organ function parameters including serum aspartate transaminase (AST) and blood urea nitrogen (BUN) contents were also measured. Results At 2 hours after CLP, STAT1 activities were found to be enhanced rapidly in the liver, lungs and small intestine, peaking at 6-24 hours, but their increase was delayed in the kidneys. Compared with STAT1, STAT3 activities were weaker and detected only in the liver and lungs, with no detectable STAT3 in the small intestine and kidneys. Pretreatment with either AG490 or RPM significantly lowered STAT1 activities in the liver, lungs and small intestine as well as STAT3 activities in the liver and lungs (P0.05). Conclusions These data suggest that abdominal infection can result in intensive activation of STAT1 and STAT3 in vital organs, and they play important roles in the pathogenesis of sepsis. Inhibition of JAK/STAT pathway can attenuate multiple organ dysfunction secondary to CLP-induced sepsis in rats.