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Chidamide-induced accumulation of reactive oxygen species

6 Elevated levels of ROS cause damage to DNA, proteins, and lipids. 7 Tumour cells produce high levels of ROS, which maintain pro-tumourigenic signalling and resistance to apoptosis. However, toxic levels of ROS production in cancers can also activate anti-tumourigenic signalling, resulting in oxidative stress-induced tumour cell death. 8 Therefore, therapies that can eliminate ROS or elevate ROS production are potential effective cancer therapies. There is an inherent vulnerability in MM cells that high rates of immunoglobulin synthesis resulting in the high level of ROS. This provides a therapeutic potential for MM. 9 Recently, studies revealed that lenalidomide triggers antitumour activities in MM primarily by targeting cereblon (CRBN) and inducing ROS-mediated oxidative stress. IKZF1 and IKZF3 are essential transcription factors in multiple myeloma.

Vascular Smooth Muscle Cells via JNK/c-JUN Pathway

Purpose: The deposition of hydroxyapatite (HAp) crystals plays an important role in the development of vascular calcification (VC). This study aimed to demonstrate the effects of nanosized HAp (nHAp) on vascular smooth muscle cells (VSMCs) and VC progression. Methods: Transmission electron microscopy (TEM) was used to examine cellular uptake of nHAp. Cell viability was determined using CCK-8 assay kit. Mitochondrial impairment and reactive oxygen species were detected by TEM and fluorescence dye staining, respectively. Cell apoptosis was detected by Western blot analysis and Annexin V staining. Mouse model of VC was built via applying nHAp on the surface of abdominal aorta. Calcification was visualized by Alizarin red and von Kossa staining.

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