Objective To investigate the protective effect of ligustrazine on the transporting function of hepatocellular mitochondria membrane in the rats with sepsis-induced acute liver injury (SALI). Methods The Sprague-Dawley (SD) rats were randomly divided into sham operation group, SALI group [established by cecal ligation and puncture (CLP)], ligustrazine treatment group (injection of ligustrazine 60 mg/kg through tail vein after CLP) and ligustrazine preventive group (7 days before CLP, ligustrazine was injected daily through tail vein for 60 mg/kg), and there were 12 rats in each group. Abdominal aorta blood and liver were harvested at 10 hours after operation. The content of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and mitochondrial aspartate aminotransferase (m-AST) were determined by enzyme coupling rate method. The content of ATP was detected by colorimetric and chemical fluorescein method. The activity of mitochondrial ATPase was detected by phosphorus quantification. The expressions of mitochondrial membrane aquaporin 8 (AQP8) and carnitine palmitoyl transferase (CPT) were detected by Western Blot. Results Compared with sham operation group, the levels of serum ALT, AST and m-AST were significantly increased in SALI group, ligustrazine treatment group and ligustrazine preventive group, and the content of ATP was reduced, the activity of mitochondrial membrane ATPase, the expressions of AQP8 and CPT-1A were significantly decreased. Compared with SALI group, the levels of serum ALT, AST and m-AST were significantly decreased in ligustrazine treatment and ligustrazine preventive groups [ALT (U/L): 123.8±32.8, 105.0±44.5 vs. 233.0±110.1; AST (U/L):427.0±117.9, 303.9±110.3 vs. 742.6±441.4; m-AST (U/L): 239.6±64.9, 168.2±60.0 vs. 412.8±252.6; all P <0.01], the content of ATP were significantly increased (nmol/mg: 29.5±10.3, 34.6±11.2 vs. 19.3±8.8, both P < 0.01), the activity of ATPase in hepatocellular mitochondrial membrane were significantly increased [Na+-K+-ATPase (U/mg):3.91±0.30, 3.97±0.35 vs. 2.87±0.82; Mg2+-ATPase (U/mg): 3.75±0.38, 3.88±0.35 vs. 2.64±1.06; Ca2+-ATPase (U/mg): 3.15±0.58, 2.98±0.31 vs. 1.75±1.25; Ca2+-Mg2+-ATPase (U/mg): 3.82±0.31, 3.91±0.42 vs. 2.57±1.01, all P < 0.01], the expressions of AQP8 and CPT-1A were significantly increased [percentage increase from sham operation group (100%), AQP8/COX-Ⅳ: (79.12±7.79)%, (88.40±9.22)% vs. (62.08±11.91)%; CPT-1A/COX-Ⅳ:(87.92±10.06)%, (84.91±17.48)% vs. (72.11±7.82)%, all P < 0.01]. The levels of serum AST and m-AST in ligustrazine preventive group were significant lower than those in ligustrazine treatment group [AST (U/L): 303.9± 110.3 vs. 427.0±117.9; m-AST (U/L): 168.2±60.0 vs. 239.6±64.9, both P < 0.05]. There was no significant difference in the expression of CPT-2 in mitochondrial membrane between the four groups. Conclusions Ligustrazine could play a protective role on the mitochondrial membrane function of transporting water, ion and fat in the rats with SALI. The preventive function of ligustrazine is better than the treatment effect of the rats with sepsis.

Objective To investigate the risk factors of acute kidney injury (AKI) occurring in patients with critical neurological disease, and the related factors affecting their prognosis. Methods The clinical data of 207 patients with critical neurological disease admitted to the Department of Critical Care Medicine of Anhui Provincial Hospital Affiliated to Anhui Medical University (South District) from January 2016 to March 2017 were analyzed retrospectively, they were assigned into an AKI group (40 cases) and a non-AKI group (167 cases), and according to the prognosis, the patients with AKI were subdivided into a survival subgroup (14 cases) and a death subgroup (26 cases). Clinical data of Glasgow coma score (GCS), acute physiology and chronic health evaluation Ⅱ (APACHEⅡ), blood glucose, white blood cell count (WBC), central venous pressure (CVP), blood sodium, cystatin C, urea nitrogen (BUN) etc. index levels and the proportions of patients using glycerin fructose and furosemide before occurrence of AKI were collected. The indexes with statistical significant differences found in the univariate analysis were analyzed by multivariate logistic regression analysis to screen out the risk factors influencing the occurrence of AKI and the factors related to the prognosis of the AKI patients; the receiver operating characteristic curve (ROC) was drawn to assess the predictive value of risk factors in patients with severe neurological disease to develop AKI. Results The incidence of AKI was 19.3% (40/207) in the patients with critical neurological disease. The hospital mortality in AKI group was significantly higher than that in the non-AKI group [65.0% (26/40) vs. 22.2% (37/167), P < 0.01]. Compared with non-AKI group, GCS (4.44±1.65 vs. 5.39±1.62), CVP [cmH2O (1 cmH2O = 0.098 kPa): 7.69±2.66 vs. 8.98±2.56] were obviously lower in AKI group at admission, APACHEⅡ(24.50±3.67 vs. 20.05±4.42), blood glucose (mmol/L: 12.33±6.53 vs. 9.33±3.26), serum sodium (mmol/L: 144.75±10.85 vs. 140.58±5.23), WBC (×109/L: 16.15±6.25 vs. 12.79±4.22), Cystatin C (mg/L: 1.27±0.74 vs. 0.74±0.26) and BUN (mmol/L: 7.81±3.33 vs. 5.53±3.20) and proportion of male [77.5% (31/40) vs. 59.9% (100/167)], patients with the comorbidity of hypotension [37.5% (15/40) vs. 19.8% (33/167)], use of glycerin fructose [17.5% (17/40) vs. 3.6% (6/167)], or use of furosemide [70.0% (28/40) vs. 13.8%(6/167)] were significantly increased in AKI group, there was a statistically significant difference between the above two groups (all P < 0.05). Multivariate logistic regression analysis showed that the hyperglycemia [odds ratio (OR) = 1.201, 95% confidence interval (95%CI) = 1.01-1.42, P < 0.05] and use of furosemide for treatment (OR = 24.493, 95%CI =4.92-120.36, P < 0.01) were the independent risk factors for occurrence of AKI in critical neurological patients. ROC curve analysis showed that blood sugar had certain predictive value of developing AKI in patients with critical neurological disease, the area under the ROC curve (AUC) of blood glucose was 0.733, when the optimal cut-off value of blood glucose was 9.05 mmol/L, the sensitivity was 77.5% and the specificity was 62.6%. Compared with the survival subgroup in the patients with AKI, the GCS at admission in death subgroup was significantly lower (3.77±0.87 vs. 5.50±2.03), but their levels of blood glucose (mmol/L: 16.51±9.10 vs. 10.09±2.89) and BUN (mmol/L: 10.26±3.07 vs. 6.48±2.70) were obviously higher than those in the survival subgroup (all P < 0.05). Conclusion AKI is one of the common complications in patients with critical neurological disease, hyperglycemia and the use of furosemide are the independent risk factors of occurrence of AKI in such patients; the blood glucose has moderate predictive value; and lower GCS, higher glucose and BUN levels in AKI patients may enhance their risk of death.