2020.02.04文献

2020.02.04文献

P (研究人群/动物) C57BL6/J male mice (8-10 weeks old)

I(干预措施) AB+with or without 1% DMB for 6 weeks

C (对照措施) Sham+with or without 1% DMB for 6 weeks

O (结果)Cardiac function, plasma TMAO level, cardiac hypertrophy and fibrosis, expression of inflammatory, susceptibility to ventricular arrhythmia and p65 NF-κB and TGF-β1/Smad3 signaling pathway were prevented by DMB treatment at the 6th week after AB surgery

思考

  1. 心功能只有射血分数、血液动力学指标缓解了,但是病理指标都缓解了,可靠否?
  2. 机制也是只观察了现象
  3. 没有细胞实验

P In Vivo: Sprague-Dawley rats weighing 180 to 200 g; In Vitro: SD rats of 3–5 days old

I In Vivo: ISO 5 mg/kg, for 2 weeks;In Vitro: 1 μg/ml of LPS for 5.5 h, and then cultured for 5 h by adding 5 ng/ml of ATP

C In Vivo: normal saline for 2 weeks; In Vitro :PBS

O DNMT1 methylation silencing of LncRNA GAS5 could lead to cardiac fibroblast pyroptosis
and activated the NLRP3, thus promoting the progression of cardiac fibrosis.

思考

  1. LncRNA与甲基化就是一个siRNA和一个甲基酶抑制剂就证明有相互关系了吗?
  2. 敲低或者过表达 LncRNA GAS5 的时候为什么没有LPS+敲低或者过表达组,只有Control NC Si/PcNDA组?

P In Vivo:ten healthy male Sprague Dawley (SD) rats weighed 250 ± 20 g In Vitro: H9C2 cells (an embryonic rat myocardium-derived cell line)

I In Vivo: abdominal aortic constriction (AAC)+injected with or without siRNA-SLC26A4 (2.5 ul) once a day for seven days.; In Vitro:PE (200 mM) for 48 h+SLC26A4 siRNA or the control siRNA

C In Vivo: Sham+ normal saline for for seven days; In Vitro :PBS?++SLC26A4 siRNA or the control siRNA

O Inhibiting SLC26A4 could decrease the release of ANP or BNP and promote the expression of GSK-3beta in vivo and in vitro.

思考

  1. 动物试验中没有sham+siRNA组
  2. 动物试验中没有心功能缓解的情况.只有个Mrna和病理缓解情况
  3. 结论中"SLC26A4 increases cardiac hypertrophy,"文中并没有做过表达实验,如何得到这个结论?
  4. GSK-3beta这个指标能够提到beta-MHC?

跟我们的研究好像没啥关系,没看了

PS

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