Publications by authors named "Mei-dong Liu"
Article Synopsis
- - The study investigated whether nicorandil can improve heart remodeling after a heart attack (myocardial infarction) and explored the mechanisms behind its effects.
- - Results showed that nicorandil reduced heart enlargement, lessened cell death in heart tissue, and inhibited fibrosis by enhancing the expression of nucleolin and promoting autophagy, while also influencing specific signaling pathways.
- - The findings suggest that nicorandil aids recovery from heart attacks by promoting autophagy and regulating key signaling molecules, which enhances heart function and reduces damage.
Article Synopsis
- Endotoxemia can lead to systemic inflammatory response syndrome (SIRS), coagulation issues, and acute lung injury (ALI), driven by activation of key blood and vascular cells.
- The study investigated the role of P-selectin glycoprotein ligand 1 (PSGL-1) using a mouse model of endotoxemia induced by lipopolysaccharide (LPS), while also administering PSGL-1 antibodies.
- Results indicated that blocking PSGL-1 reduced platelet and leukocyte activity, lessened inflammation, improved survival rates, and mitigated lung damage in the endotoxemic mice, highlighting PSGL-1's significant contribution to these conditions.
Article Synopsis
- Clopidogrel is a medication that inhibits platelet activation and aggregation, which is important during inflammation and endotoxemia (a severe immune response).
- The study investigated how clopidogrel affects inflammation in mice after inducing it with lipopolysaccharide (LPS), focusing on platelet and leukocyte activation and their interactions.
- Results showed that clopidogrel reduced lung damage, platelet-neutrophil aggregates, and inflammatory markers, suggesting it effectively dampens platelet activation and overall inflammation in endotoxemic conditions.
Article Synopsis
- The study investigated how puerarin affects vascular endothelial cell injury caused by lipopolysaccharide (LPS), focusing on the mechanisms behind this effect.
- Using various assays, the researchers evaluated cell viability, morphological changes, and levels of inflammatory markers in cell culture supernatants.
- The results showed that puerarin treatment reduced the harmful effects of LPS on endothelial cells by lowering inflammatory marker levels and inhibiting the activation of NF-κB, which is associated with inflammation.
MicroRNA Profiling of Transgenic Mice with Myocardial Overexpression of Nucleolin.
Chin Med J (Engl)
February 2018
Article Synopsis
- - Nucleolin (NCL) is an essential RNA-binding protein involved in various cellular functions like chromatin stability and ribosome assembly, but its specific actions on microRNA (miRNA) expression are not well understood.
- - The study created transgenic mice that overexpress NCL in the heart to analyze changes in miRNA profiles, revealing 11 miRNAs were upregulated and 4 downregulated compared to wild-type mice, confirmed by further testing.
- - The findings suggest that the protective effects of NCL on heart cells may be linked to the miRNAs identified, indicating a potential regulatory role for NCL in cardiac health.
Article Synopsis
- The study investigated the role of up-regulated protein 2 (MIP2) in cardioprotection during IPoC, showing that MIP2 levels significantly increased in both in vivo and in vitro models following IPoC treatment.
- Results indicated that higher MIP2 expression reduced heart damage and apoptosis after injury, while blocking MIP2 with siRNA in H9c2 cells diminished the protective effects, showing its critical role in IPoC-mediated cardioprotection.
[Effect of Krüppel-like factor 4 overexpression on heat stress-induced apoptosis of Raw264.7 macrophages].
Zhong Nan Da Xue Xue Bao Yi Xue Ban
December 2007
Article Synopsis
- The study aimed to investigate how overexpressing the protein KLF4 affects cell death (apoptosis) in macrophages when subjected to heat stress.
- Researchers inserted the KLF4 gene into a vector and introduced it into Raw264.7 macrophages, then analyzed the cells after exposing them to heat stress.
- Results showed that macrophages with higher KLF4 levels had significantly increased apoptosis after heat stress, indicated by various assays confirming cell death and DNA fragmentation.
[Effect of HSP72 on acute injury of neonatal cardiomyocytes induced by oxidative stress].
Zhong Nan Da Xue Xue Bao Yi Xue Ban
April 2006
Objective: To explore the protective effect of HSP72 on the acute injury of cardiomyocyte induced by oxidative stress.
Methods: Cardiomyocytes of neonatal rats treated with heat shock (42 degrees C, 30 min, recovery for 6 h) to induce the expression of HSP72 and HSP72 antisense oligonucleotide was transformed to block the expression of HSP72. 0.
[Immortalization of embryonic fibroblasts in heat shock transcription factor 1 knockout mouse].
Zhong Nan Da Xue Xue Bao Yi Xue Ban
April 2006
Article Synopsis
- - The study aimed to create immortalized embryonic fibroblast cell lines from both HSF1-deficient (HSF1-/-) and normal (HSF1+/+) mice to investigate the role of heat shock factor 1 (HSF1).
- - Researchers used a specific vector to introduce SV40 large T antigen into the fibroblasts and confirmed successful integration and expression of this gene in both cell lines via various techniques.
- - After six months of cultivation, the HSF1+/+ and HSF1-/- fibroblast lines displayed stable growth, but HSP70, a protein typically induced by heat shock, was not activated in the HSF1-/- cells.
[HSF1 inhibits heat stress-induced apoptosis in Raw264.7 macrophages].
Zhong Nan Da Xue Xue Bao Yi Xue Ban
April 2006
Objective: To observe the effect of heat shock factor 1 (HSF1) on heat stress-induced apoptosis in Raw264.7 macrophages.
Methods: Raw264.
[Characteristics and expression of Mip5, a novel gene associated with myocardial ischemia/reperfusion in rats].
Zhong Nan Da Xue Xue Bao Yi Xue Ban
October 2005
Objective: To determine the characteristics of a novel gene Mip5 (GenBank accession number AY553870) and its expression under physiological and pathological conditions.
Methods: The characteristics of Mip5 were analyzed by bioinformatic programs including BLAST, spidey, psort, ClustalW and so on. RT-PCR was performed to detect Mip5 expression.
[Roles of nuclear factor-kappaB in heat shock pretreatment to abate cardiomyocyte injury induced by hydrogen peroxide].
Zhongguo Wei Zhong Bing Ji Jiu Yi Xue
July 2005
Objective: To investigate the role of nuclear factor-kappaB (NF-kappaB) in heat shock pretreatment to abate cardiomyocyte injury induced by hydrogen peroxide (H(2)O(2)).
Methods: The primary generation of cultured neonatal rat cardiomyocytes were injured by exposure to 1 mmol/L H(2)O(2) for different durations. The total antioxidant in cardiomyocytes was detected.
[Effect of nucleolin down-regulation on the proliferation and apoptosis in C2C12 cells].
Zhong Nan Da Xue Xue Bao Yi Xue Ban
April 2005
Objective: To clarify the effect of nucleolin on the proliferation and apoptosis in C2C12 cells.
Methods: After inhibiting the expression of nucleolin using antisense oligonucleotides, the cellular proliferation was determined by MTT, and the apoptosis was detected by flow cytometry (FCM) assays and DNA ladder assays.
Results: After being transfected with antisense oligonucleotides for 24 hours, Western blotting showed that the expression of nucleolin was repressed significantly.
[HSP70 inhibits smac release from the mitochondria and protects against H2O2-induced apoptosis in C2C12 myogenic cells].
Zhong Nan Da Xue Xue Bao Yi Xue Ban
February 2005
Article Synopsis
- The study aimed to determine if HSP70 can protect C2C12 myogenic cells from apoptosis induced by hydrogen peroxide (H2O2) by preventing the release of Smac from mitochondria.
- The researchers used various methods, including gene transfection and Western blotting, to analyze protein levels, check for apoptotic changes, and measure caspase activities associated with apoptosis.
- Results showed that HSP70 overexpression significantly reduced apoptosis and inhibited Smac release, indicating its protective role against H2O2-induced cell death in these muscle cells.