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Acute gangrenous cholecystitis is a histologic diagnosis,mostly diagnosed by intraoperative or postoperative pathology.In China,as the aging population increases,the incidence of the disease increases steadily.AGC is still an indication of surgical treatment for acute cholecystitis(AC),but the diagnosis and treatment of AGC remains a challenge for clinical surgeons.However,preoperative clinical data such as age, gender,hypertension,diabetes,coronary heart disease,cholelithiasis disease history,laboratory examination and radiographic results are helpful in early diagnosis and reasonable surgical timing selection.
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Acute gangrenous cholecystitis is a histologic diagnosis,mostly diagnosed by intraoperative or postoperative pathology.In China,as the aging population increases,the incidence of the disease increases steadily.AGC is still an indication of surgical treatment for acute cholecystitis(AC),but the diagnosis and treatment of AGC remains a challenge for clinical surgeons.However,preoperative clinical data such as age, gender,hypertension,diabetes,coronary heart disease,cholelithiasis disease history,laboratory examination and radiographic results are helpful in early diagnosis and reasonable surgical timing selection.
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Objective To explore the relationship between platelet to lymphocyte ratio (PLR) and microangiopathyin type 2 diabetes mellitus. Methods In this case-control study, the clinical data on 428 adult patients with type 2 diabetic microangiopathy in our hospital from January 2009 to December 2015 were retrospectively analyzed. PLR, age, sex, fasting blood glucose, glycosylated hemoglobin, total cholesterol and triglyceride were tested to investigate their relationship with type 2 diabetic microangiopathy. Results Logistic regression analysis showed that PLR was a risk factor of type 2 diabetic microangiopathy (OR = 3.162, 95%CI:1.556 ~ 7.421, P < 0.05). Conclusions Greater PLR is closely related to type 2 diabetic microangiopathy, and we should pay attention to type 2 diabetic microangiopathy with a greater PLR in clinical practice.
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ObjectiveTo investigate the preventive effects of rosiglitazone on nonalcoholic steatohepatitis (NASH) rats and to explore the potential mechanisms in modulating peroxisome proliferator-activated receptor gamma (PPARγ),nuclear factor kappa B (NF-κB),and cyclooxygenase-2 (COX-2) expression.Methods Thirty male SD rats were assigned into the normal group ( n =10),the model group ( n =10),rosiglitazone prevention group [ n =10,simultaneously 4mg/( kg · d) gavage daily at beginning].Liver appearance,liver index,and histological changes were assessed.Serum tumor necrosis factor-o (TNF-c) and prostaglandin E2 (PGE2) were determined using enzyme-linked immunosorbent assay.The expressions of PPARγ,NF-κB,and COX-2 in liver were determined using immunohistochemical methods.The mRNA and protein expressions of COX-2 were disclosed by real-time polymerase chain reaction and Western blot analysis.ResultsCompared with the normal group,the liver index significantly increased in model group (3.92 ±0.72 vs.5.71 ± 1.05,P =0.004).HE and Masson staining showed significantly increased steatosis,inflammation,and fibrosis.The serum levels of TNF-α,PGE2 in high-fat-diet-fed rats were significantly increased ( 11.72 ± 2.47 vs.29.39 ± 5.32,P =0.002 ; 236.60 ± 24.90vs.288.24 ± 17.17,P =0.004).Immunohistochemistry showed NF-κB and COX-2 in livers were significantly elevated,but PPARγ wasdecreased in nonalcoholic steatohepatitis rats.Real-time polymerase chain reaction and Western blot found mRNA and protein expressions of COX-2 were increased in the model group (0.57 ± 0.08 vs.2.83 ± 0.24,P =0.0007 ; 0.38 ± 0.03 vs.1.00 ± 0.03,P =0.004).Compared with the model group,the expressions of PPARγsignificantly increased and the expressions of NF-κB and COX-2 significantly decreased ( mRNA:2.83 ± 0.24 vs.0.46 ± 0.11,P =0.002 ; protein: 1.00 ± 0.03 vs.0.62 ± 0.02,P =0.006 ) in the rosiglitazone prevention group.ConclusionBy inhibiting NF-κB and COX-2 expressions,rosiglitazone can reduce insulin resistance and then prevent the occurrence and deve lopment of nonalcoholic steatohepatitis.
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Objective To investigate the effects of icarrin on the activity and protein expression of core binding factor otl(Cbfa1) in rat osteoblasts cultured in vitro,and to explore whether mitogen-activated protein kinase (MAPK) pathway is involved in this process.Methods Calvarial osteoblasts were obtained from newborn (<24 h) SD rats by trypsin-coUagenase digestion method.The second generation osteoblasts were cultured in the medium containing icariin (10 ng/ml) or estradiol (10-8 mol/L) with or without extracellular-signal regulated kinase (ERK) inhibitor (UO126) or p38MAPK inhibitor (SB203580).Nuclear protein was extracted from osteoblasts.And then the activity of Cbfa1 was detected by ELISA.The amounts of Cbfa1 protein were detected by Western blot.Results Calvarial osteoblasts were obtained successfully and were used in this study after indentified by alkaline phosphatase and mineralized nodus staining.Cbfa1 expression and the activity in osteoblasts were up-regulated by both icariin and estradiol (P<0.05).The effects were partly inhibited by addition of U0126or SB203580 (P<0.05).Conclusions Either icarrin or estradiol can stimulate the proliferation and maturation of cultured osteoblasts in vitro via up-regulating the activity and expression of Cbfal.The MAPK signal pathway inhibitor seems to partly decrease Cbfa1 activity.It suggests that MAPK pathway may be involved in the transduction of icariin's impact on proliferation and mineralization of osteoblasts.
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Objective To evaluate the impact of rosiglitazone (Ros) on liver expression of peroxisome proliferator-activated receptor γ (PPARγ),nuclear factor (NF-κB) and cyclooxygenase-2(COX-2) in treatment of nonalcoholic steatohepatitis (NASH) rats.Methods Thirty Sprague-Dawley rats were divided into normal group,model group and Ros treated group with 10 each.Except the normal group,the other two groups were given high fat diet for 12 weeks for NASH model.The rats in Ros treated group were gavaged 4 mg/kg of Ros daily at the 12th week for 8 weeks.All rats were sacrificed at the 20th week for blood sample and liver tissue.Biochemical parameters of liver function,lipid metabolism,glycometabolism and antioxidant enzyme activities were measured.The histological change of the liver were assessed with HE and Masson staining.The level of tumor necrosis factor (TNF)-α and prostaglandin E2 (PGE2) was measured using ELISA.The expression of PPARγ,NF-κB and COX-2 was detected with immunohistochemistry.The mRNA and protein expressions of COX-2 were tested by real-time PCR and Western blotting,respectively.Results In comparison with model group,Ros treated group showed significant improvement in hepatic steatosis,inflammation and fibrosis(all P value<0.05).In model group,the serum levels of fasting blood glucose,insulin and HOMA-insulin resistance index (HOMA-IRI),total cholesterol (TC),total triglyeride (TG),lowdensity lipoprotein cholesterol (LDL-C) and free fatty acids were increased,but HDL-C level was decreased.All above parameters markedly improved after Ros treatment.The levels of ALT and AST,total anti-oxidation competence,superoxide dismutase,catalase,glutathione peroxidase and malondialdehyde in Ros treated group were significantly ameliorated when compared with those in model group.Immunohistochemistry showed that the expression of NF-κB and COX-2 was significantly elevated,but PPARγ was decreased in model group.Real-time PCR and Western blot revealed that the mRNA and protein expressions of COX-2 were higher in the model group than those in normal group (0.57±0.08 vs 0.38±0.03;2.83±0.24 vs 1.00±0.03,P=0.000 and P=0.004,respectively),but significantly lower in Ros treated group (0.55±0.06 and 1.84±0.13,P<0.01).Conclusions Ros can reduce oxidative stress and insulin resistance in NASH rats by activing PPARγ expression and inhibiting expression of NF-κB and cyclooxygenases.