Myocardial caspase-3 and NF-κB activation promotes calpain-induced septic apoptosis: The role of Akt/eNOS/NO pathway

Luo, Rong; Chen, Xuepin; Ma, Huihui; Yao, Chao; Liu, Mingjiang; Jian-hong, Tao; Li, Xiaoping

doi:10.1016/j.lfs.2019.02.048

Cited by 29 publications

(18 citation statements)

References 32 publications

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“…The present study reported that rosuvastatin significantly suppressed apoptosis of HCAECs through regulation of the JAK2/STAT3 pathway. A previous study noted that myocardial caspase-3 activation promotes calpain-induced septic apoptosis ( 42 ). Another study indicated that decreasing cleaved-caspase-9 expression inhibits myocardial cell apoptosis during myocardial ischemia-reperfusion injury in rats ( 43 ).…”

Section: Discussionmentioning

confidence: 99%

Statin rosuvastatin inhibits apoptosis of human coronary artery endothelial cells through upregulation of the JAK2/STAT3 signaling pathway

Wang¹,

Li²,

Xie³

et al. 2020

Mol Med Rep

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The purpose of the present study was to explore the potential molecular signaling pathway mediated by the statin rosuvastatin in cultured human coronary artery endothelial cells (Hcaecs) induced by cocl 2. cocl 2 was used to induce the apoptosis of Hcaecs. Myocardial infarction rats were established and received statin or PBS treatment. reverse transcription-quantitative Pcr, western blotting, eliSa, Tunel assay and immunohistochemistry were used to analyze the role of statin treatment. The results showed that rosuvastatin treatment decreased apoptosis of Hcaecs induced by cocl 2 by increasing anti-apoptosis Bcl-xl and Bcl-2 expression, and decreasing pro-apoptosis Bax, Bad, caspase-3 and caspase-9 expression. The myocardial ischemia rat model demonstrated that rosuvastatin treatment decreased the mitochondrial reactive oxygen species, inflammation, mitochondrial damage, lipid catabolism, heart failure and the myocardial infarction areas, but improved the cardiac function indicators, right and left ventricular ejection fraction and increased expression levels of Janus kinase (JaK) and signal transducer and activator of transcription (STaT)3 in myocardial tissue. in conclusion, the results of the current study revealed that the statin rosuvastatin presents cardioprotective effects by activation of the JaK2/STaT3 signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Statin rosuvastatin inhibits apoptosis of human coronary artery endothelial cells through upregulation of the JAK2/STAT3 signaling pathway

Wang¹,

Li²,

Xie³

et al. 2020

Mol Med Rep

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“…[31] Tumour cells evade apoptosis by abnormally stimulating the pro-apoptotic and antiapoptotic proteins in a variety of ways. [32] Caspase is a protease that promotes apoptosis, [33] which is at the core of the network of apoptotic mechanisms. [34] Caspase activation and caspase cascade can be regulated by a variety of apoptosis-inhibiting signals, such as Bcl-2 family, calpain and Ca 2+ .…”

Section: Discussionmentioning

confidence: 99%

1-(4-((5-chloro-4-((2-(isopropylsulfonyl)phenyl)amino)pyrimidin-2-yl)amino)-3-methoxyphenyl)-3-(2-(dimethylamino)ethyl)imidazolidin-2-one (ZX-42), a novel ALK inhibitor, induces apoptosis and protective autophagy in H2228 cells

Wang

Liu

et al. 2020

Journal of Pharmacy and Pharmacology

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Objectives To examine the antiproliferative effects of 1‐(4‐((5‐chloro‐4‐((2‐(isopropylsulfonyl)phenyl)amino)pyrimidin‐2‐yl)amino)‐3‐methoxyphenyl)‐3‐(2‐(dimethylamino)ethyl)imidazolidin‐2‐one (ZX‐42) on the echinoderm microtubule‐associated protein‐4/anaplastic lymphoma kinase fusion gene (EML4‐ALK) positive lung cancer cell line H2228 and its underlying mechanism. Methods The MTT assay was used to study the effect of ZX‐42 on H2228 cell growth. Propidium iodide (PI) staining and Western blotting were used to investigate the cell cycle changes. ZX‐42‐induced cell apoptosis was determined using the Annexin V‐FITC/PI (AV/PI) apoptotic assay kit, acridine orange/ethidium bromide (AO/EB) and Hoechst 33258 staining, Rhodamine 123 (Rh 123) fluorescence assay and Western blotting. ZX‐42‐induced reactive oxygen species (ROS) production was examined by ROS assay kit. Transmission electron microscope, monodansylcadaverine (MDC) staining and the AV/PI apoptotic assay kit were used to demonstrate the relationship between autophagy and apoptosis. Key findings ZX‐42 had good cell viability inhibitory effect on H2228 cells. ZX‐42 dramatically inhibited ALK and its downstream pathways. ZX‐42 also blocked H2228 cell cycle at G1 phase and then induced apoptosis by activating the mitochondrial pathway. Next, ZX‐42 induced the production of ROS, and antioxidant N‐acetylcysteine (NAC) reduced ROS production and also decreased apoptotic rates. We also found that ZX‐42 induced protective autophagy in H2228 cells. Conclusions In summary, ZX‐42 is a novel ALK inhibitor that significantly inhibits the cell viability of H2228 cells and ultimately induces apoptosis through the mitochondrial pathway, in which autophagy plays a protective role. Therefore, inhibition of autophagy might enhance the anti‐cancer effect of ZX‐42.

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“…3n and o), indicating that the drugs are triggering apoptosis and thus killing cancer cells. Although initially contradictory, activation of Akt (primarily a survival pathway) is known to kill cancer cells through the direct phosphorylation and activation of eNOS, leading to nitric oxide production and ultimately triggering apoptosis 43 . Here, we found that eNOS phosphorylation at S1177 was enhanced in the tumors from the animals treated with SA or ASA ( Fig.…”

Section: Resultsmentioning

confidence: 99%

Acetylsalicylic acid and salicylic acid present anticancer properties against melanoma by promoting nitric oxide-dependent endoplasmic reticulum stress and apoptosis

Ausina

Branco

Demaria

et al. 2020

Sci Rep

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Melanoma is the most aggressive and fatal type of skin cancer due to being highly proliferative. Acetylsalicylic acid (ASA; Aspirin) and salicylic acid (SA) are ancient drugs with multiple applications in medicine. Here, we showed that ASA and SA present anticancer effects against a murine model of implanted melanoma. These effects were also validated in 3D- and 2D-cultured melanoma B16F10 cells, where the drugs promoted pro-apoptotic effects. In both in vivo and in vitro models, SA and ASA triggered endoplasmic reticulum (ER) stress, which culminates with the upregulation of the pro-apoptotic transcription factor C/EBP homologous protein (CHOP). These effects are initiated by ASA/SA-triggered Akt/mTOR/AMPK-dependent activation of nitric oxide synthase 3 (eNOS), which increases nitric oxide and reactive oxygen species production inducing ER stress response. In the end, we propose that ASA and SA instigate anticancer effects by a novel mechanism, the activation of ER stress.

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Myocardial caspase-3 and NF-κB activation promotes calpain-induced septic apoptosis: The role of Akt/eNOS/NO pathway

Cited by 29 publications

References 32 publications

Statin rosuvastatin inhibits apoptosis of human coronary artery endothelial cells through upregulation of the JAK2/STAT3 signaling pathway

Statin rosuvastatin inhibits apoptosis of human coronary artery endothelial cells through upregulation of the JAK2/STAT3 signaling pathway

1-(4-((5-chloro-4-((2-(isopropylsulfonyl)phenyl)amino)pyrimidin-2-yl)amino)-3-methoxyphenyl)-3-(2-(dimethylamino)ethyl)imidazolidin-2-one (ZX-42), a novel ALK inhibitor, induces apoptosis and protective autophagy in H2228 cells

Acetylsalicylic acid and salicylic acid present anticancer properties against melanoma by promoting nitric oxide-dependent endoplasmic reticulum stress and apoptosis

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