ABSTRACT
ObjectiveTo investigate the association of liver stiffness measurement (LSM) and serum biochemical parameters with hepatic steatosis, liver inflammation, and liver fibrosis in patients with nonalcoholic steatohepatitis (NASH). MethodsA total of 520 patients with NASH who were treated in The Fifth Medical Center of Chinese PLA General Hospital from January 2007 to December 2018 were enrolled, and according to body mass index (BMI) with a cut-off value of 28 kg/m2, the patients were divided into obese group with 151 patients and non-obese group with 369 patients. All patients underwent liver biopsy, and LSM was measured within 3 days before biopsy. Serum biochemical parameters and general clinical data were collected before liver biopsy, and the noninvasive indices aspartate aminotransferase to platelet ratio index (APRI) and fibrosis-4 (FIB-4) were calculated. The t-test was used for comparison of normally distributed continuous between groups, the nonparametric Mann-Whitney U test was used for comparison of non-normally distributed continuous between groups; the chi-square test was used for comparison of categorical data between groups. A Spearman rank correlation analysis was also performed. ResultsAlanine aminotransferase (ALT), aspartate aminotransferase, LSM, controlled attenuation parameter (CAP), spleen length, and APRI gradually increased with the increase in BMI (all P＜0.05). The Spearman correlation analysis showed that LSM, ALT, BMI, and CAP were positively correlated with the degree of hepatic steatosis (r=0.263, 0.327, 0.184, and 0.452, all P＜0.05); LSM, ALT, and CAP were positively correlated with the degree of liver inflammation (r=0.357, 0.278, and 0.121, all P＜0.05); LSM, ALT, BMI, and CAP were positively correlated with the degree of liver fibrosis (r=0.500, 0.216, 0.248, and 0.101, all P＜0.05); age was negatively correlated with the degree of hepatic steatosis, liver inflammation, and liver fibrosis (r=-0.344, -0.129, and -0.163, all P＜0.05). ConclusionLSM, CAP, ALT, and age are significantly correlated with the degree of liver inflammation, liver fibrosis, and hepatic steatosis in NASH patients, and therefore, they can be used in noninvasive diagnostic and predictive models to access the severity of liver injury.
ABSTRACT
OBJECTIVE:To study the protective effects of Danshen injection on 5/6 nephrectomiy induced model rats with in-flammatory renal injury. METHODS:50 rats were equally randomized into a sham-operation (isometric distilled water) group,a model (isometric distilled water) group,a positive control [captopril 5 mg/(kg·d)] group and Danshen injection low-dose and high-dose [1.6,4.8 ml/(kg·d)] groups. Models were established by performing 5/6 nephrectomy on the rats in all groups except the sham-operation group. The rats were given drugs for 4 consecutive weeks from the 6th week. 24 h urine protein was determined for all rats every week. After the last administration,the contents of creatinine,urea nitrogen and interleukins 1β(IL-1β),IL-2 and IL-10 in rats’serum were determined. Pathological changes and infiltration of macrophages CD68 in rats’kidney tissues were ob-served. RESULTS:Compared to the sham-operation group,those in the model group had more 24 h urine protein and more obvi-ous renal pathologic changes during 1-4 weeks of administration,and higher contents of creatinine,urea nitrogen,IL-1β,IL-2 and IL-10 and CD68 positive expression in serum. Compared to the model group,during 2-4 weeks of administration,those in the posi-tive control group and Danshen injection low-dose and high-dose groups had less 24 h urine protein,milder renal pathologic chang-es,and lower contents of creatinine,urea nitrogen,IL-1β and CD68 positive expression in serum,and higher content of IL-10, and only the rats in the positive control group demonstrated lower IL-2 content. There of the above were statistical differences(P<0.01 or P<0.05). CONCLUSIONS:Danshen injection can alleviate renal pathologic changes and reduce inflammatory injury of the kidneys of 5/6 nephrectomiy induced model rats.
ABSTRACT
Neutrophils play an essential role in the innate immune response to infection. Neutrophils migrate from the vasculature into the tissue in response to infection. Recently, a neutrophil cell surface receptor, CD177, was shown to help mediate neutrophil migration across the endothelium through interactions with PECAM1. We examined a publicly available gene array dataset of CD177 expression from human neutrophils following pulmonary endotoxin instillation. Among all 22,214 genes examined, CD177 mRNA was the most upregulated following endotoxin exposure. The high level of CD177 expression is also maintained in airspace neutrophils, suggesting a potential involvement of CD177 in neutrophil infiltration under infectious diseases. To determine the role of CD177 in neutrophils in vivo, we constructed a CD177-genetic knockout mouse model. The mice with homozygous deletion of CD177 have no discernible phenotype and no significant change in immune cells, other than decreased neutrophil counts in peripheral blood. We examined the role of CD177 in neutrophil accumulation using a skin infection model with Staphylococcus aureus. CD177 deletion reduced neutrophil counts in inflammatory skin caused by S. aureus. Mechanistically we found that CD177 deletion in mouse neutrophils has no significant impact in CXCL1/KC- or fMLP-induced migration, but led to significant cell death. Herein we established a novel genetic mouse model to study the role of CD177 and found that CD177 plays an important role in neutrophils.