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This study aimed to evaluate the therapeutic efficacy and effect of blood purification (BP) therapy on severe acute pancreatitis (SAP). Information on 305 patients (BP group 68, control group 237) diagnosed with SAP was retrieved from the Medical Information Mart for Intensive Care IV (MIMIC IV) database. Firstly, the influence of BP treatment was preliminarily evaluated by comparing the outcome indicators of the two groups. Secondly, multiple regression analysis was used to screen the mortality risk factors to verify the impact of BP on the survival outcome of patients. Then, the effect of BP treatment was re-validated with baseline data. Finally, cox regression was used to make the survival curve after matching to confirm whether BP could affect the death outcome. The results indicated that the BP group had a lower incidence of shock (p = 0.012), but a higher incidence of acute kidney injury (AKI) (p < 0.001), with no differences observed in other outcome indicators when compared to the control group. It was also found that the 28-day survival curve of patients between the two groups was significantly overlapped (p = 0.133), indicating that BP treatment had no significant effect on the survival outcome of patients with SAP. Although BP is beneficial in stabilizing hemodynamics, it has no effect on short- and long-term mortality of patients. The application of this technology in the treatment of SAP should be done with caution until appropriate BP treatment methods are developed, particularly for patients who are not able to adapt to renal replacement therapy.

Abstract Acute pancreatitis is characterized by zymogen preactivation. Severe inflammation caused by zymogen activation can eventually lead to multiple organ dysfunctions which contribute to the high mortality rate of severe acute pancreatitis. However, there is no specific treatment available for acute pancreatitis therapy. Here, we show that spautin-1, which effectively inhibits autophagy flux, ameliorated the pathogenesis of acute pancreatitis induced by cerulein or L-arginine. CaMKII phosphorylation due to cytosolic calcium overload was revealed in this paper. It was also demonstrated that autophagic protein aggregates degradation blockade accompanied by impaired autophagy correlated positively with intra-acinar cell digestive aymogen activation stimulated by cerulein or L-arginine. The role of spautin-1 in ameliorating acute pancreatitis was shown here to be associated with impaired autophagy inhibition and Ca2+ overload alleviation. We provide a promising therapy for acute pancreatitis through targeting both impaired autophagy and increased cytosolic calcium.

Aims: Effect and mechanism of Yulangsan flavonoid (YLSF) on rat myocardial ischemia/reperfusion injury (MI/RI) has been investigated. Methods: Sprague-Dawley (SD) rats were randomly divided into seven groups (sham group, model group and NS group: 2 mL of normal saline/kg body weight was administered; diltiazem group: 5 mg of diltiazem hydrochloride/kg body weight was administered; YLSFL, YLSFM and YLSFH groups: 20, 40 and 80 mg of YLSF/kg body weight was administered) and the MI/RI model was established. Myocardial infarct area, levels of myocardial enzymes and nitric oxide synthase (NOS) were measured. Caspase-3 and adenine nucleotide translocator-1 (ANT1) mRNA expression were evaluated by reverse transcription polymerase chain reaction (RT-PCR). Pathological structure and cardiocyte ultrastructure were also analysed. Results: Compared with the MI/RI group, pretreatment with YLSF or diltiazem hydrochloride decreased the infarct area, levels of inducible nitric oxide synthase (iNOS), caspase-3 as well as the leakage of myocardial enzyme and increased activities of total nitric oxide synthase (tNOS) as well as constitutive nitric oxide synthase (cNOS). Cellular edema and the infiltration of inflammatory cells were alleviated. Conclusions: The experiment showed that YLSF protected the heart against MI/RI, possibly by reducing lipid peroxidation damage, regulating NOS activity and modulating the apoptosis genes expression.

[Objectives] To investigate the protective effect of ethanol extract from sweet potato leaves on liver injury induced by CC14 in mice. [Methods] 25 ICR mice were randomly divided into blank group, model group, high-dose extract group (200 mg/kg), low-dose extract group (100 mg/kg) and positive control group (2 mg/kg colchicine), with 5 mice in each group. All groups except the blank group were given intraperitoneal injection of 20% CC14 olive oil solution (2 mL/kg), and the blank group was given the same dose of olive oil solution three times a week. After 4 weeks, each administration group was given the corresponding dose of drugs (10 mL/kg), and the blank group and model group were given the corresponding amount of normal saline for 2 weeks. After the last intragastric administration, fasting was required, but water was allowed, blood was taken from eyeballs, and upper serum was taken by static centrifugation. Serum AST, ALT, CRP, IL-6 and SOD levels were detected by the kit. [Results] Compared with the blank group, the serum AST and ALT levels in the model group were significantly increased; compared with the model group, the ethanol extract of sweet potato leaves could decrease the levels of ALT, AST, CRP, IL-6 and increase the level of SOD in serum. [Conclusions] The ethanol extract of sweet potato leaves had protective effect on the mice with liver injury induced by CC14, and its mechanism may be to protect the liver by lowering enzymes, inhibiting inflammation and antioxidant stress. [ABSTRACT FROM AUTHOR]

The article discusses a study on a mouse model of depression induced by unpredictable chronic mild stress. The study used Yulangsan polysaccharide (YLSPS) to treat the model mice. It performed enzyme-linked immunosorbent assay, radioimmunity and immunohistochemical staining following the treatment. It showed the inhibition of depression by YLSPS by upregulating monoamine neurotransmitters and prefrontal cortex adenylate cyclase activity.