Glycolipid Metabolism Disorder in the Liver of Obese Mice Is Improved by TUDCA via the Restoration of Defective Hepatic Autophagy

Objective. Tauroursodeoxycholic acid (TUDCA) has been considered an important regulator of energy metabolism in obesity. However, the mechanism underlying how TUDCA is involved in insulin resistance is not fully understood. We tested the effects of TUDCA on autophagic dysfunction in obese mice. Material and Methods. 500 mg/kg of TUDCA was injected into obese mice, and metabolic parameters, autophagy markers, and insulin signaling molecular were assessed by Western blotting and real-time PCR. Results. The TUDCA injections in the obese mice resulted in a reduced body weight gain, lower blood glucose, and improved insulin sensitivity compared with obese mice that were injected with vehicle. Meanwhile, TUDCA treatment not only reversed autophagic dysfunction and endoplasmic reticulum stress, but also improved the impaired insulin signaling in the liver of obese mice. Additionally, the same results obtained with TUDCA were evident in obese mice treated with the adenoviral Atg7. Conclusions. We found that TUDCA reversed abnormal autophagy, reduced ER stress, and restored insulin sensitivity in the liver of obese mice and that glycolipid metabolism disorder was also improved via the restoration of defective hepatic autophagy

Hepatic infarction induced by HELLP syndrome: a case report and review of the literature

Abstract Background HELLP syndrome is a rare disease in China, and 20% of patients with severe preeclampsia have been accompanied with HELLP syndrome, which is characterized by the presence of hemolysis, elevated liver enzymes and low platelet count. Case presentation In this case, we reported that a patient with preeclampsia was diagnosed with HELLP syndrome. Furthermore, hepatic infarction also was found via the computed tomographic (CT) images, which showed peripheral wedge-shaped inhomogeneous low attenuation in the right hepatic lobes via plain CT scan, and the low-density shadow and mottled appearance in the same areas where vessels were seen coursing through them via contrast-enhanced CT scan. Conclusions Besides typical clinical manifestations of the pregnant patient with preeclampsia, the typical laboratory evidences were elevated liver enzymes and thrombocytopenia. The abdominal CT scan showed imaging features of hepatic infarction, which was helpful to identify the rare complication of HELLP syndrome. Thus, we diagnosed a patient with HELLP syndrome with hepatic infarction, though the patient had no chance to do the liver biopsy

Biomechanical responses of the cornea after small incision lenticule extraction (SMILE) refractive surgery based on a finite element model of the human eye

Purpose: To investigate the biomechanical responses of the human cornea after small incision lenticule extraction (SMILE) procedures, especially their effects of SMILE surgery on stress and strain. Methods: Based on finite element analysis, a three-dimensional (3D) model of the human eye was established to simulate SMILE refractive surgery procedures. Stress and strain values were calculated by inputting the intraocular pressure (IOP). Results: After SMILE refractive surgery procedures, the stress and strain of the anterior and posterior corneal surfaces were significantly increased. The equivalent stress and strain on the anterior and posterior corneal surfaces increased with increasing diopter and were concentrated in the central area, whereas the values of stress and strain at the incision site on the anterior surface of the cornea were approximately 0. Compared with the anterior corneal surface, the stress and strain of the posterior surface were larger. Increasing IOP caused an approximately linear change in stress and a nonlinear increase in corneal strain. In addition, we found that the incision sizes and direction had less of an influence on stress and strain. In summary, SMILE surgery increased the equivalent stress and strain on the human cornea. Conclusions: The equivalent stress and strain of the anterior and posterior human corneal surfaces increased after SMILE refractive surgery; these increases were particularly noticeable on the posterior surface of the cornea

Tunicamycin aggravates endoplasmic reticulum stress and airway inflammation via PERK-ATF4-CHOP signaling in a murine model of neutrophilic asthma

<p><i>Introduction</i>: Endoplasmic reticulum (ER) stress has been considered to be an important regulator of airway inflammation in the pathogenesis of bronchial asthma, but the mechanism of ER stress involved in neutrophilic asthma remain not fully understood. <i>Methods</i>: Tunicamycin is a mixture of homologous nucleoside antibiotics, which is used to induce ER stress. In the present study, Tunicamycin was administered to mouse bronchial epithelial cells and a neutrophilic asthma model (OVA_LPS-OVA mice), and ER stress indicators and inflammatory cytokines were measured by Western blotting and Elisa. <i>Results</i>: Tunicamycin not only induced ER stress in mouse bronchial epithelial cells, but also increased expression of inflammation indicators such as IL-6, IL-8, and TNF-α via PERK-ATF4-CHOP signaling. Additionally, the phosphorylation of PERK and the expression levels of ATF4 and CHOP proteins and inflammatory cytokines (IL-6, IL-8 and TNF-α) were elevated in the lung tissue of OVA_LPS-OVA mice. Administering tunicamycin further increased protein expression levels of ER stress indicators and inflammatory cytokines, and resulted in more severe asthma phenotypes in OVA_LPS-OVA mice, suggesting that PERK-ATF4-CHOP signaling is associated with airway inflammation in neutrophil-dominant asthma. <i>Conclusions</i>: These data support the emerging notion that regulation of ER stress could be strongly associated with the development of neutrophilic asthma.</p