Leonurine protects against influenza A virus infection-induced pneumonia in mice.

Influenza A virus (H1N1), a swine-origin influenza A virus, causes seasonal epidemics that result in severe illnesses and deaths. Leonurine has been reported to function as an anti-inflammatory agent with protective effects on nervous, urinary and cardiovascular systems. However, the therapeutic effects of leonurine on the pneumonia caused by H1N1 infection remain unclear. Hematoxylin and eosin staining was performed to evaluate the lung injuries of mice infected by H1N1. The amount of immune cells was analyzed by flow cytometry. Enzyme-linked immunosorbent assay was used to evaluate the alteration of multiple cytokines in lung tissues. Real-time quantitative polymerase chain reaction assay was performed to investigate the ribonucleic acid (RNA) levels of certain genes. The protein levels in toll-like receptor 4/nuclear factor kappa-light-chain-enhancer of activated B cells (TLR4/NF-κB) signaling were estimated by western blot assay. Leonurine treatment significantly inhibited the mortality caused by H1N1 infection. Leonurine treatment (60 mg/kg) alleviated the lung injuries caused by virus infection. The inflammatory cell accumulation and cytokine expression were inhibited by the leonurine administration. Leonurine inhibited the mRNA expression of pro-inflammatory cytokines in the lung homogenates at day 5 postinfection. Leonurine regulated the TLR4/NF-κB signaling in the lung homogenates of H1N1-infected mice at day 5 postinfection. Leonurine protects against H1N1 infection-induced pneumonia in mice.

LINC01354 Promotes Osteosarcoma Cell Invasion by Up-regulating Integrin ß1.

BACKGROUND AND AIMS: Long noncoding RNAs have been proved to play a key role in the development and progression of various tumors, including osteosarcoma (OS). However, the role and molecular mechanism of lncRNA in osteosarcoma metastasis remains unknown. Our purpose is to explore the clinical significance and biological function of LINC01354 in osteosarcoma. METHODS: Expression of LINC01354 in OS tissues, serum and cell lines was measured and the association between LINC01354 expression and clinicopathological factors was analyzed. The functional effects of LINC01354 were examined in vitro by using transwell assays, western blot, immunohistochemistry (IHC) and in vivo in a xenograft tumor mouse model. RESULTS: LINC01354 was overexpressed in OS tissues, serum and cells. LINC01354 overexpression promoted OS cells invasion, EMT and integrin ß1 expression, while knockdown of LINC01354 inhibited OS cell invasion, epithelial-mesenchymal transition (EMT) and integrin ß1 expression. In addition, integrin-ß1 blockage with MAB13 antibody abrogated the effects of LINC01354 overexpression on promoting OS cells invasion and EMT. In addition, LINC01354 promoted OS cell metastasis in vivo. CONCLUSION: LINC01354 promote OS cell EMT and invasion through up-regulating integrin ß1. Our study suggested that LINC01354 may be regarded as a potential target for the clinical treatment of OS.

Comparison of Efficiency of TACE plus HIFU and TACE alone on Patients with Primary Liver Cancer.

OBJECTIVE: To compare efficiency of trans-arterial chemo-embolization (TACE) plus high intensity focused ultrasound (HIFU), and TACE alone on patients with primary liver cancer. STUDY DESIGN: A descriptive, analytical study. PLACE AND DURATION OF STUDY: Department of Ultrasound, Daqing Oilfield General Hospital, China, from March 2015 to March 2017. METHODOLOGY: A total of 90 primary liver cancer patients were randomly divided into control group and observation group, 45 cases in each group. Control group was treated with TACE alone, while observation group was treated with HIFU plus TACE. Alpha-fetoprotein (AFP), alanine amino-transferase (ALT), aspartate amino-transferase (AST), total bilirubin (TBIL), and frequency of complications, were compared in the two groups. RESULTS: The total remission rate of observation group was higher than that of control group (p=0.017). At 6 months after treatment, AFP level in observation group was lower than that in control group (p <0.001). There was no statistical difference in liver function indicators of ALT, AST, and TBIL between two groups (p=0.968, 0.944 and 0.973, respectively). The incidence of digestive tract hemorrhage was lower than that in control group (p=0.049). After one year of follow-up, the tumor recurrence rate and tumor metastasis rate in observation group were lower than that of control group (p=0.036 and 0.044, respectively). CONCLUSION: Treatment of primary liver cancer by TACE plus HIFU has a higher overall remission rate, causes little damage to normal liver tissue, can fully kill tumor cells and reduce postoperative local recurrence and metastasis rate with less adverse reactions.

Quercetin attenuates mitochondrial dysfunction and biogenesis via upregulated AMPK/SIRT1 signaling pathway in OA rats.

Despite the severity of osteoarthritis (OA), current medical therapy strategies for OA aim at symptom control and pain reduction, as there is no ideal drug for effective OA treatment. OA rat model was used to explore the therapeutic function of quercetin on remission of OA, by determining the reactive oxygen species (ROS) levels, mitochondrial function and extracellular matrix integrity. Quercetin could attenuate ROS generation and augment the glutathione (GSH) and glutathione peroxidase (GPx) expression levels in OA rat. Quercetin not only enhanced mitochondrial membrane potential, oxygen consumption, adenosine triphosphate (ATP) levels in mitochondria, but also increased the mitochondrial copy number. Furthermore, the interlukin (IL)-1ß-induced accumulation of nitric oxide (NO), matrixmetalloproteinase (MMP)-3) and MMP-13 could be suppressed by quercetin. Finally, we confirmed that the therapeutic properties of quercetin on OA might function through the adenosine monophosphate-activated protein kinase/sirtuin 1 (AMPK/SIRT1) signaling pathway. In summary, quercetin could alleviate OA through attenuating the ROS levels, reversing the mitochondrial dysfunction and keeping the integrality of extracellular matrix of joint cartilage. The underlying mechanism might involve the regulation of AMPK/SIRT1 signaling pathway.