Objective To explore the impact of different doses of butylphthalide on renal interstitial fibrosis in mice with obstructive nephropathy, and to discuss the correlation between Nrf-2 expression level and renal interstitial fibrosis. Methods Totally 72 male CD-1 mice of clean grade were selected and randomly assigned into 4 groups:sham operation group (Sham), model group (UUO), low dose of butylphthalide group (NBPL) and high dose of butylphthalide group (NBPH). In addition to the control group, UUO model was established in other three groups. NBPL group was given NBP 150 mg/(kg· d) by gavage since postoperative day 1,NBPH group was given NBP 220 mg/(kg·d) by gavage. Sham group and UUO group were given equal volume of saline by gavage. Six mice were sacrificed at the third, 7th, 14th day, respectively. The obstructive renal tissue was selected for immunohistochemical staining and Western blot assay. The expression levels of Nrf- 2 and type Ⅰ collagen were detected by Western blot assay. Results The IOD value of type Ⅰ collagen was increased with time in UUO group, and which showed a gradual decreasing trend in Sham group, NBPL group and NBPH group (P<0.05). The IOD values at different time points were significantly higher in UUO group, NBPL group and NBPH group compared to those of Sham group. The IOD values were significantly decreased in NBPL and NBPH groups than that of UUO group, and IOD value was lower in NBPH group than that of NBPL group (P<0.05). Western blot assay showed that IOD values of Nrf-2 and type Ⅰ collagen at 7 d and 14 d were increased in UUO group, NBPL group and NBPH group compared with those of Sham group. The IOD values of Nrf-2 protein were increased, and IOD values of type Ⅰcollagen were decreased, in NBPL group and NBPH group than those of UUO group. The IOD value of Nrf-2 protein was decreased in NBPL group than that of NBPH group, but the IOD value of type Ⅰcollagen was increased in NBPL group than that of NBPH group (P<0.05). Conclusion NBP can improve renal interstitial fibrosis in UUO mice, which may be related with the increased expression of Nrf-2 and the down-regulated expression of type I collagen.

Objective To study on the possible mechanism of butylphthalide delaying renal fibrosis of mice with obstructive nephropathy. Methods Totally 72 male CD-1 mice of clean grade were selected and randomly assigned into 4 groups: sham operation group (Sham), model group (UUO), control group (ACEI) and treatment group (NBP). The mice in the control group (ACEI) and the treatment group (NBP) were given benazepril and butylphthalide by gavage, and the mice in sham operation group (Sham) and model group (UUO) were given normal saline by gavage. Six mice were sacrificed at the third, 7th, 14th day, respectively. The obstructive renal tissue was selected for immunohistochemical staining and western blot. Results (1)With the longer time of ureteral obstruction, the expression of Nrf-2 was gradually strengthened in time-dependent manner;(2)Compared with the model group, the levels of Nrf-2 and γ-GCS in butylphthalide group were significantly increased, and the expression of type Ⅰ collagen was decreased significantly (P < 0.05). The expression of Nrf-2 and γ-GCS in each time points was stronger than that in the benazepril group (P < 0.05). Correlation analysis showed that: there was a positive correlation between Nrf-2 and γ-GCS (r = 0.930) and a negative correlation between Nrf-2 and the expression level of type Ⅰ collagen(r = -0.859). Conclusion Butylphthalide can relieve renal interstitial injury caused by oxidative stress and delay the progress of renal interstitial fibrosis by activation of Nrf-2 pathway and up-regulated expression ofγ-GCS.

Objective To explore the rule of the Nrf2-ARE in renal interstitial fibrosis and the mechanism of butylphthalide on renal protective effect.Methods Seventy-two male CD-1 mice were divided into 4 groups,Sham group,UUO group,NBP group,ACEI group.The Sham group and UUO group were gavaged with physiological saline.The NBP group was gavaged with butylphthalide.The ACEI group was gavaged with benazepril.After 3,7,14 days,6 mice were executed and collection of kidney tissue.The expression of Nrf2,γ-GCS and type Ⅰ collagen were detected by immunohistochemisty,RT-PCR and Western blot.The correlation of Nrf2 and γ-GCS was assessmented by linear regression.Results The expression of type Ⅰ collagen in UUO group was increased compared with the Sham group,However,the expression of Type Ⅰ collagen in NBP group or ACEI group were reduced compared with the UUO group.Compared with Sham group,the expression of Nrf2mRNA,γ-GCSmRNA and type Ⅰ collagen mRNA in uuogroup were increased in 3,7,14 days after surgery.Compared with UUO group at 7th,14u day,the lelve of Nrf2 mRNA were apparently increased in NBP group (P＜0.05).It was a positive correlation between the Nrf2 and γ-GCS and negative correlation between the γ-GCS and Type Ⅰ collagen.Conclusion The renal protective effect of butylphthalide in the renal interstitial fibrosis was more predominant than benazepril.The roles maybe occurred through increased the expression of Nrf2 and γ-GCS and alleviated the expression of Type Ⅰ collagen in nephridial tissue.

ObjectiveTo explore the relationship among the aggressive behavior,hostile attribution bias and childhood trauma in schizophrenic patients.Methods 135 schizophrenic patients were tested with Modified Overt Aggression Scale (MOAS),the Chinese-version of the Ambiguous Intentions Hostility Questionnaire (AIHQ-C) and Childhood Trauma Questionnaire (CTQ).According to the score of the MOAS,the patients were divided into the aggressive group ( n =58 ) and the non-aggressive group ( n =77 ).The hostile attribution bias and the childhood trauma were compared between the two groups,and correlation and hierarchical regression analysis were used to investigate the relationships of the variables.ResultsCompared with the non-aggressive patients,the aggressive patients had significantly higher AIHQ-C total hostility bias score (6.27 ± 1.20 vs 5.90 ± 0.97,P ＜0.05 ),total blame bias score (8.04 ± 1.97 vs 6.91 ± 2.10,P ＜ 0.01 ) and total aggression bias score ( 6.17 ±1.02 vs 5.59 ± 1.04,P ＜ 0.01 ).Correlation analysis showed that the MOAS score,AIHQ scores and the total score of CTQ were significantly positively correlated with each other ( r =0.171 ～ 0.350,P ＜ 0.05 ～0.01 ).Regression analysis indicated the hostile attribution bias directly predicted the aggressive behavior( β =0.342,P ＜0.05) and completely mediated the relationship between the childhood trauma and the aggressive behavior.ConclusionThe aggressive behavior in schizophrenic patients is associated with the experience of childhood trauma and the attribution style.The childhood trauma indirectly influences the aggressive behavior by the mediating of the hostile attribution bias.

The prevalence rate of nonalcoholic fatty liver disease (NAFLD) is increasing year by year, which poses a heavy burden on global public health. The pathogenesis of NAFLD is closely associated with the factors including obesity, insulin resistance, and diet, among which diet is the core and cornerstone of the prevention and treatment of NAFLD. In view of the fact that previous studies focused on the association of different dietary components, structures, and plans with NAFLD and seldom explored the impact of overall dietary behavior on NAFLD, this article reviews the effect of dietary behavior on NAFLD, in order to provide a reference for the prevention and treatment of NAFLD and the guidance on rational dietary behaviors and habits for patients.

objectiveTo investigate the differences in clinical indices and lipid metabolism between the patients with nonalcoholic fatty liver disease （NAFLD） and healthy individuals in the overweight population. MethodsIn this study， body mass index （BMI）>23 kg/m² was defined as overweight. A total of 62 overweight patients with NAFLD who were admitted to Putuo Hospital Affiliated to Shanghai University of Traditional Chinese Medicine from August 2020 to April 2021 were enrolled as overweight NAFLD group， and 50 overweight individuals who underwent physical examination during the same period of time were enrolled as control group. Clinical information and blood biochemical parameters were recorded for all subjects. Ultra-performance liquid chromatography-tandem mass spectrometry was used to analyze serum lipidomic profile， and principal component analysis and orthogonal partial least squares-discriminant analysis were used to perform the multivariate statistical analysis of lipidomic data. The chi-square test was used for comparison of categorical data between two groups， and the independent-samples t test or the Wilcoxon rank-sum test was used for comparison of continuous data between two groups. ResultsThe overweight NAFLD group had a significantly higher BMI than the overweight control group （Z=-2.365， P=0.018）. As for serological markers， compared with the overweight control group， the overweight NAFLD group had significantly higher levels of red blood cells， hemoglobin， hematocrit， uric acid， total protein， globulin， alkaline phosphatase， gamma-glutamyl transpeptidase， alanine aminotransferase， aspartate aminotransferase， cholinesterase， low-density lipoprotein， total cholesterol， triglyceride， apolipoprotein B， and blood glucose （all P<0.05）. The lipidomic analysis showed that there was a significant difference in lipid metabolism between the two groups， and a total of 493 differentially expressed lipids were identified （VIP value>1， P<0.05）， among which 143 lipids were significantly upregulated and 350 lipids were significantly downregulated in the overweight NAFLD group. The mean total fatty acid content in the overweight NAFLD group was 3.6 times that in the overweight control group. Compared with the overweight control group， the overweight NAFLD group had a significant reduction in the content of triglyceride with>3 unsaturated bonds （P<0.001） and a significant increase in the content of triglyceride with ≤3 unsaturated bonds （P<0.001）. ConclusionCompared with healthy overweight individuals， overweight NAFLD patients tend to have significant abnormalities in some biochemical parameters and lipid metabolites， with significant increases in the content of fatty acid in blood and the types of saturated fat chains in triglycerides.