Protective effects of alpha lipoic acid on high glucose-induced neurotoxicity in PC12 cells

Colorectal cancer (CRC) is one of the most leading cancer deaths throughout the world. MiR-200c has been shown to have a critical role in cancer initiation and progression. In this study, we investigated the miR-200c expression in CRC tissues and its effects on CRC cell lines which were mediated by polycomb complex protein (BMI1). Quantitative reverse transcription polymerase chain reaction (QRT-PCR) and immunohistochemistry were used to detect miR-200c and BMI1 expression in tumor tissues from 38 patients with CRC and 38 normal colon tissues. HCT-116 and SW-48 cells were transfected by locked nucleic acid (LNA)-anti-miR-200c. Western blot analysis and real-time PCR were applied to determine the BMI1 protein and microRNA (miRNA) levels. The apoptosis was analyzed via annexin/propidium iodide staining, and cell invasion was evaluated by transwell assay. MiR-200c was markedly downregulated in CRC tissues, whereas the protein expression of BMI1 in CRC tissues was upregulated compared with normal colon tissues. In the colon cancer cell lines, transfection of LNA-anti-miR-200c increased BMI1 gene and protein expression as well as the cell invasion. Downregulation of miR-200c by LNA decreased the apoptotic cells. The results from this study revealed that miR-200c may have antitumor effects through inhibition of BMI1 expression.

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“…20 Fifty microgram protein was loaded onto a 12% SDS-PAGE and transferred on a nitrocellulose membrane.…”

Section: Western Blot Analysismentioning

confidence: 99%

Retracted: Anticancer effects of miR‐200c in colorectal cancer through BMI1

Mazraehshah

Tavangar

Saidijam

et al. 2018

J of Cellular Biochemistry

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“…PC12 cell, a mature cell line from a rat pheochromocytoma, has been widely used in neurophysiological studies. In particular, these cells have served as a commonly used cellular model for studying the mechanisms underlying glucose neurotoxicity [ 21 – 23 ]. With regard to Lipin1, results from in vitro experiments which have shown that Lipin1 concentrations were reduced when PC12 cells were treated with HG and Lipin1 alleviated HG-induced neurotoxicity in these cells.…”

Section: Discussionmentioning

confidence: 99%

Lipin1 Is Involved in the Pathogenesis of Diabetic Encephalopathy through the PKD/Limk/Cofilin Signaling Pathway

Xie

Wang

Liu

et al. 2020

Oxidative Medicine and Cellular Longevity

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Diabetic encephalopathy is a type of central diabetic neuropathy resulting from diabetes mainly manifested as cognitive impairments. However, its underlying pathogenesis and effective treatment strategies remain unclear. In the present study, we investigated the effect of Lipin1, a phosphatidic acid phosphatase enzyme, on the pathogenesis of diabetic encephalopathy. We found that in vitro, Lipin1 exerts protective effects on high glucose-induced reductions of PC12 cell viability, while in vivo, Lipin1 is downregulated within the CA1 hippocampal region in a type I diabetes rat model. Increased levels of Lipin1 within the CA1 region are accompanied with protective effects including amelioration of dendritic spine and synaptic deficiencies, phosphorylation of the synaptic plasticity-related proteins, LIM kinase 1 (p-limk1) and cofilin, as well as increases in the synthesis of diacylglycerol (DAG), and the expression of phosphorylated protein kinase D (p-PKD). These effects are associated with the rescue of cognitive disorders as shown in this rat model of diabetes. In contrast, knockdown of Lipin1 within the CA1 region enhanced neuronal abnormalities and the genesis of cognitive impairment in rats. These results suggest that Lipin1 may exert neuroprotective effects involving the PKD/Limk/Cofilin signaling pathway and may serve as a potential therapeutic target for diabetic encephalopathy.

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“…In addition AA administration significantly reduced MDA and SOD levels and significantly improved the activities of GPX and SOD in liver and brain tissues. The protective effect of ALA is derived from its ability to counteract ROS generation and exhibited beneficial role in the treatment of chronic liver diseases [24]. ALA treatment of HE -induced rats significantly decremented serum TNF-α and S100-β levels.…”

Section: Discussionmentioning

confidence: 99%