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991.
X.M. Wang S.J. Gao X.F. Guo W.J. Sun Z.Q. Yan W.X. Wang Y.Q. Xu D. Lu 《Brazilian journal of medical and biological research》2014,47(4):273-278
Overexpression of cytokine-induced apoptosis inhibitor 1 (CIAPIN1) contributes to
multidrug resistance (MDR) in breast cancer. This study aimed to evaluate the
potential of CIAPIN1 gene silencing by RNA interference (RNAi) as a
treatment for drug-resistant breast cancer and to investigate the effect of
CIAPIN1 on the drug resistance of breast cancer in
vivo. We used lentivirus-vector-based RNAi to knock down
CIAPIN1 in nude mice bearing MDR breast cancer tumors and found
that lentivirus-vector-mediated silencing of CIAPIN1 could
efficiently and significantly inhibit tumor growth when combined with chemotherapy
in vivo. Furthermore, Western blot analysis showed that both
CIAPIN1 and P-glycoprotein expression were efficiently downregulated, and P53 was
upregulated, after RNAi. Therefore, we concluded that lentivirus-vector-mediated RNAi
targeting of CIAPIN1 is a potential approach to reverse MDR of
breast cancer. In addition, CIAPIN1 may participate in MDR of breast
cancer by regulating P-glycoprotein and P53 expression. 相似文献
992.
Y. Wang J.J. Mu F.Q. Liu K.Y. Ren H.Y. Xiao Z. Yang Z.Y. Yuan 《Brazilian journal of medical and biological research》2014,47(3):223-230
Dietary salt intake has been linked to hypertension and cardiovascular disease. Accumulating evidence has indicated that salt-sensitive individuals on high salt intake are more likely to develop renal fibrosis. Epithelial-to-mesenchymal transition (EMT) participates in the development and progression of renal fibrosis in humans and animals. The objective of this study was to investigate the impact of a high-salt diet on EMT in Dahl salt-sensitive (SS) rats. Twenty-four male SS and consomic SS-13BN rats were randomized to a normal diet or a high-salt diet. After 4 weeks, systolic blood pressure (SBP) and albuminuria were analyzed, and renal fibrosis was histopathologically evaluated. Tubular EMT was evaluated using immunohistochemistry and real-time PCR with E-cadherin and alpha smooth muscle actin (α-SMA). After 4 weeks, SBP and albuminuria were significantly increased in the SS high-salt group compared with the normal diet group. Dietary salt intake induced renal fibrosis and tubular EMT as identified by reduced expression of E-cadherin and enhanced expression of α-SMA in SS rats. Both blood pressure and renal interstitial fibrosis were negatively correlated with E-cadherin but positively correlated with α-SMA. Salt intake induced tubular EMT and renal injury in SS rats, and this relationship might depend on the increase in blood pressure. 相似文献
993.
High-quality evidence suggests that aspirin is a promising agent for cancer prevention and treatment. Direct inhibition of cyclooxygenase-2 (COX-2) pathway is generally thought to be the main mechanism by which aspirin inhibits cancer development. However, either pharmacological properties of aspirin or recent results of epidemiologic studies do not support that mechanism. To address this inconsistency, we hypothesize that antiplatelet effect of aspirin via inhibition of COX-1 may be one of potential mechanisms to inhibit carcinogenesis. Aberrant platelet activation will lead to promote hostility of tumor microenvironment by releasing an abundant array of angiogenesis regulators. 相似文献
994.
Recent data have shown that the purinergic receptor P2X4 plays key roles in inflammatory responses. We evaluated whether P2X4 inhibition could affect the development of arthritis and autoimmunity in collagen-induced arthritis (CIA) model. P2X4 antisense oligonucleotide (asODN) was injected intravenously via tail vein into the CIA mice to selectively inhibit P2X4 expression daily for 14 days. P2X4 asODN treatment reduced the clinical score of CIA in mice. P2X4 asODN also decreased the levels of serum IL-1β, TNF-α, IL-6, and IL-17. P2X4 asODN treatment significantly inhibited synovial inflammation and joint destruction. P2X4 asODN treatment also suppressed the NLR family, pyrin domain containing 1 (NLRP1) inflammasome activation in CIA mice and synovial cells of human rheumatoid arthritis. These data show that P2X4 asODN confers a therapeutic benefit on CIA. Inhibition of the NLRP1 inflammasome signaling pathway is the underlying mechanism of action. 相似文献
995.
996.
Yuanyuan Zhang Mingchuan Liu Ruiping Fan Qianliu Zhou Jinping Yang Shengjie Yang Chaojih Wang Junping Kou 《RSC advances》2019,9(69):40736
Air pollution is an increasingly serious problem, and the fine particles of air pollution can cause diseases of the respiratory, cardiovascular, and immune systems. Walnut protein isolates (WPIs) are peptides purified from walnut protein hydrolysates that have very high antioxidant and 1,1-diphenyl-2-picrylhydrazyl radical 2,2-diphenyl-1-(2,4,6-trinitrophenyl)hydrazyl (DPPH) scavenging activities. In this study, mice and zebra fish were used to test the effect of WPIs on the acute lung injury (ALI) and heart injury induced by particulate matter (PM). The WPIs protected against ALI in the PM-induced ALI mouse model by inhibiting myeloperoxidase (MPO), nitric oxide (NO), interleukin 1β(IL-1β), and interleukin 6(IL-6) in ALI mouse bronchoalveolar lavage fluid (BALF) and pro-inflammatory cytokine production and acyl carrier protein (ACP) level. In the zebra fish model, the WPIs promoted the secretion of PM into the intestinal tract, protected against the heart injury caused by PM, and promoted the phagocytosis of zebra fish macrophages. Therefore, WPIs are potential candidates to be a health-promoting product with no toxicity.This study supports new prospects for WPI development and shows WPIs may be potential candidates for healthy products. 相似文献
997.
998.
999.
M. P. Oryszczyn J. Godin C. Frette G. Hellier J. P. Bertrand Q. T. Pham F. Kauffmann 《American journal of industrial medicine》1996,30(3):281-284
Selenium (Se) plasma levels were studied 222 coal miners to assess whether selenium is decreased in relation to coal dust exposure, taking age, alcohol, and tobacco consumption into account. Selenium levels decreased significantly with age and current tobacco consumption, among miners aged 34–50. Long-term and current exposure to coal dust were studied. The lowest Se values were observed for those with both long-term and current exposure (60.2 ng/ml), the highest for those never or slightly exposed (64.1 ng/ml); those with long-term exposure not currently exposed fell in an intermediate position (61.3 ng/ml). No relation was observed with alcohol consumption. The association of coal dust with low selenium remained significant after adjustment for age and smoking. © 1996 Wiley-Liss, Inc. 相似文献
1000.
Q.-L. Zhang P.-X. Lin D. Shi H. Xian H.deF. Webster 《Journal of neuroscience research》1996,43(4):496-502
To learn more about neuropeptide-induced glial responses which accompany axon regeneration, we studied effects of VIP on laminin production by cultured Schwann cells. Schwann cells were isolated from sciatic nerves of neonatal mice, purified, and incubated for 5 days in either control medium (DMEM + 15% FCS) or control medium containing 10−7 -10−11 M VIP. At 10−7 and 10−8 M VIP, laminin levels measured by enzyme-linked immunosorbent assay were significantly higher (55% and 35%) than those in control cultures. Lower VIP concentrations (10−9 -10−11 M) produced smaller increases which were not significant. Low-affinity VIP receptors which mediated this effect were demonstrated on Schwann cells by radioligand binding studies. The increased Schwann cell synthesis of laminin induced by VIP was blocked when either a VIP antagonist or a VIP receptor antagonist was added to the VIP-containing incubation medium. In contrast to astrocytes, when Schwann cells were loaded with fura-2, VIP did not increase cytosolic Ca2+. This indicates that Schwann cells and astrocytes may have different intracellular transduction pathways; their receptor subtypes also may differ. We suggest that the VIP-induced increase in laminin synthesis which we have observed in cultured Schwann cells may also occur in vivo and might be an important component of axon-Schwann cell interactions during nerve regeneration. © 1996 Wiley-Liss, Inc. 相似文献