Objective To observe the pathological changes of liver cells in the early periods of burn injury combined with endotoxemia and to explore its mechanisms preliminarily. Methods Rats were inflicted with 20% TBSA Ⅲ degree burn combined with intraperitoneal injection of lipopolysaccharide (burn injury combined with endotoxemia, combined group) or simply burned or simply injected. Each group included 25 rats, with 5 rats left for control. Rats in the former 3 groups were sacrificed and sampled at 1, 3, 6, 12 and 24 h after injury, 5 rats for each time point. The results were observed by HE staining, TUNEL and DNA gel electrophoresis, and the concentrations of plasma MDA and the activity of plasma SOD were assessed and analyzed. Results Apoptosis of liver cells was found in each of the 3 groups but its regularity was different from one another. Much more apoptotic cells in the combined group were found than the other 2 groups and apoptosis happened earlier with its maximum at 6 h postinjury and declined thereafter. Much less apoptotic cells were found in the simply burned group and reached the maximum at 12 h postburn. There were only a few apoptotic cells at 6 h postinjection in the simply injected group in which there were the fewest apoptotic cells in the three groups. The concentration of plasma MDA and the activity of SOD always moved in the opposite way at the same time. In the combined group, the maximum of MDA concentration and the minimum of SOD activity happened at the same time point, which was just before the one of the maximum of liver cell apoptosis. Conclusion During the early period of burn injury combined with endotoxemia, rat liver cells die mainly in the apoptotic way, with lots of apoptotic cells at 6 h and 12 h postinjury, combined with necrosis at 24 h. Lipid peroxidation may partly account for the apoptosis of liver cells.

OBJECTIVETo study the relationship between phosphatidylinositol-3-kinases(PI3K)/protein-serine-threonine kinase(AKt) signaling pathway and orthodontic tooth movement.

METHODSTwenty-four rabbits were chosen to establish rabbit models for the study. The right maxillary teeth of each animal treated by orthodontics were as the test side, and the untreated left teeth were as the control side. The animals were sacrificed at 3, 5, 7, 14 d, respectively. The prepared tissue specimens were processed for the study. The changes of the expression of PI3K, AKt in periodontal tissues were detected by real-time quantitative-polymerase chain reaction (RQ-PCR) and Western blot techniques.

RESULTSRQ-PCR showed that the expression of PI3K, AKt mRNA dramatically changed at 3 d. The expression of PI3K, AKt mRNA in the test side was higher than the control side, especially at 7 d, and then decreased. Compared with the control side, there was statistical significant difference in the test side(P < 0.05). The study obtained consistent conclusion from Western blot and RQ-PCR.

CONCLUSIONExpression of PI3K, AKt in rabbit periodontal tissues increase during orthodontic tooth movement, which prompts that PI3K/AKt signal pathways relate to orthodontic tooth movement and PI3K/AKt signal pathway involve in the periodontal tissue remodeling.

Animals ; Phosphatidylinositol 3-Kinases ; Phosphatidylinositols ; Protein-Serine-Threonine Kinases ; Proto-Oncogene Proteins c-akt ; RNA, Messenger ; Rabbits ; Signal Transduction ; Tooth Movement Techniques

Extracellular vesicles (EVs)-based cell-free strategy has shown therapeutic potential in tissue regeneration. Due to their important roles in intercellular communications and their natural ability to shield cargos from degradation, EVs are also emerged as novel delivery vehicles for various bioactive molecules and drugs. Accumulating studies have revealed that EVs can be modified to enhance their efficacy and specificity for the treatment of many diseases. Engineered EVs are poised as the next generation of targeted delivery platform in the field of precision therapy. In this review, the unique properties of EVs are overviewed in terms of their biogenesis, contents, surface features and biological functions, and the recent advances in the strategies of engineered EVs construction are summarized. Additionally, we also discuss the potential applications of engineered EVs in targeted therapy of cancer and damaged tissues, and evaluate the opportunities and challenges for translating them into clinical practice.

OBJECTIVETo investigate the effects of simvastatin on the expression of nuclear factor-κB (NF-κB) and intercellular adhesion molecule-1 (ICAM-1) in the lung tissue of rats with lung injury induced by ischemia-reperfusion (IR) of the hind limbs.

METHODSForty-eight male adult SD rats were randomized into 6 equal groups, including a sham-operated group, an IR group, 3 IR+simvastatin groups with intragastric administration of 1, 5, or 10 mg·kg(-1)·d(-1) for 3 days, and a simvastatin control group treated with 10 mg·kg(-1)·d(-1) simvastatin. IR of the hind limbs was induced in the 4 IR groups by occlusion of bilateral femoral arteries for 2 h followed by a 3-h reperfusion. The rats were sacrificed at the end of reperfusion and the arterial blood was taken for blood gas analysis. The lungs were immediately removed for pathological examination and determination of the lung Wet/dry weight ratio (W/D), myeloperoxidase (MPO) activity and polymorphonuclear neutrophil (PMN) counting. The expression of NF-κB p65 mRNA and ICAM-1 protein in the lungs was detected using RT-PCR and Western blotting.

RESULTSAlveolar edema, localized pulmonary atelectasis and large amount of PMN infiltration were found in IR group, and these changes were ameliorated in the 3 simvastatin groups (S(1), S(5), S(10)). Lung W/D, MPO activity and PMN counting were significantly increased in IR group as compared with the sham-operated group (P<0.01). Lung W/D, MPO activity and PMN counting were significantly lowered in the 3 simvastatin groups as compared with IR group (P<0.01). IR-induced decrease in PaO(2) was significantly increased in the 3 simvastatin groups (P<0.01), which also showed significantly lowered expressions of NF-κB p65mRNA and ICAM-1 protein in a dose-dependent manner (P<0.01).

CONCLUSIONSimvastatin attenuates lung injury induced by IR of the hind limbs in rats by suppressing the activation of NF-κB and subsequent accumulation of neutrophils mediated by ICAM-1.

Animals ; Hindlimb ; blood supply ; Intercellular Adhesion Molecule-1 ; genetics ; metabolism ; Ischemia ; physiopathology ; Lung ; metabolism ; Lung Injury ; etiology ; metabolism ; Male ; NF-kappa B ; genetics ; metabolism ; RNA, Messenger ; genetics ; metabolism ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; complications ; Simvastatin ; pharmacology ; Transcription Factor RelA ; genetics ; metabolism