Saurabh Kumar Jha, Niraj Kumar Jha, Rohan Kar, Rashmi Kumar Ambasta, Pravir Kumar,
Volume 4, Issue 2 (3-2015)
Abstract
Parkinson's disease (PD) is a chronic neurodegenerative condition which has the second largest incidence rate among all other neurodegenerative disorders barring Alzheimer's disease (AD). Currently there is no cure and researchers continue to probe the therapeutic prospect in cell cultures and animal models of PD. Out of several factors contributing to PD prognosis, the role of p38 MAPKs (mitogen-activated protein (MAP) kinase) and PI3K/AKT signalling module in PD brains is crucial because impaired balance between the pro-apoptotic and anti-apoptotic pathways trigger unwanted phenotypes such as microglia activation, neuroinflammation, oxidative stress, and apoptosis. These factors continue challenging the brain homeostasis in initial stages thereby essentially assisting the dopaminergic (DA) neurons towards progressive degeneration in PD. Neurotherapeutics against PD shall then be targeted against the misregulated accomplices of the p38 and PI3K/AKT cascades. In this review, we have outlined many such established mechanism involving the p38 MAPK and PI3K/AKT pathways which can offer therapeutic windows for rectification of aberrant DA neuronal dynamics in PD brains.
Beren Ateş, Çağrı Öner, Zeynep Akbulut, Ertuğrul Çolak,
Volume 11, Issue 3 (2-2022)
Abstract
Capsaicin is a natural product which is extracted from pepper and has the potential to be used in cancer treatment because of its anti- proliferative effects. The aim of the study was to determine the effect of capsaicin on the hepatocellular carcinoma cell proliferation and the expressions of related genetic markers as Ki-67, PI3K/AKT/mTOR and epigenetic markers as miR-126 and piR-Hep-1. The inhibitory concentration of capsaicin in HepG2 cells was determined. piR-Hep-1 and miR-126 expressions and Ki-67, PI3K, AKT and mTOR gene expressions were examined by RT-PCR. The inhibitory concentration of capsaicin for HepG2 cells was 200 nM and the decreased proliferation was observed at 24th hour. As epigenetic markers, an up regulation of miR-126 and down regulation of piR-Hep-1 expression were determined after treatment. Moreover, Ki-67, PI3K and mTOR gene expressions decreased while AKT gene expression increased after the treatment (p<0.001). According to the obtained data, capsaicin has an impact on proliferation both genetically and epigenetically. Furthermore, treatment of capsaicin effects miR-126 and piR-Hep-1 expressions which effect carcinogenesis in different way. Moreover, there are some clues which indicate that these two small non-coding RNA might affect each other and share the same target molecules post-transcriptionally.
