Background: Many studies have used rotenone (ROT) to create an experimental animal model of Parkinson’s disease (PD) because of its ability to induce similar behavioral and motor deficits. PD is the most common age-related motoric neurodegenerative disorder. Neuroinflammation and apoptosis play an important role in the pathogenesis of this disease.
Objective: This study investigated the effect of butanolic (n-BuOH) extract of Centaurea africana (200 mg/kg, 16 days) on a ROT-induced neurotoxicity model in male Wistar albino rats.
Methods: Estimation of Tumor Necrosis Factor (TNF-α) and Nitric Oxide (NO) levels along with the myeloperoxidase (MPO) activity in brains was carried out in order to evaluate neuro-inflammation. Oxidative stress, Caspase 3 activity (apoptosis), and behavioral alterations were also evaluated.
Results: In behavior assessment, using Ludolph Movement Analysis Scale, all ROT treated animals showed a decreased locomotor activity. The mitochondrial dysfunction induced by ROT was expressed by a decreased activity of complex I of the mitochondrial respiratory chain and increased lipid peroxidation and caspase 3. Co-treatment with the n-BuOH extract significantly restored the activity of complex I (65.41 %) compared to treatment with ROT alone. The n-BuOH extract also reduced the neuroinflammation in rat brains by reducing MPO activity (75.12 %), NO levels (77.43 %), and TNF-α (71.48 %) compared to the group treated with ROT.
Conclusion: The obtained results indicated that C. africana n-BuOH extract exhibited a protective effect in rats. Read more:https://bit.ly/3B0BvvR
Background: Since signal transducer and activator of transcription 3 (STAT3) is aberrantly activated in hepatocellular carcinoma (HCC) and plays a key role in this tumor progression. Inhibition of the STAT3 signaling pathway has been considered as an effective therapeutic strategy for suppressing HCC development.
Objective: In this study, we investigated the anti-cancer effects of EH-42 on HCC cells and tried to explain the underlying mechanism.
Methods: MTT assay, colon formation assay and AnnexinV-FITC/PI double-staining assay were performed to assess the effects of EH-42 on cell growth and survival. Wound healing assay and transwell invasion assay were performed to assess the effects of EH-42 on cell migration and invasion. Western blotting assay was performed to analyze the effects of EH-42 on relative proteins.
Results: According to the MTT assay, colon formation assay and AnnexinV-FITC/PI doublestaining assay, EH-42 could suppress the growth and induce apoptosis of HCC cells in a dosedependent manner. Further western blotting assay showed that the inhibitory effects of EH-42 on cell growth and survival were caused by activating caspase 3/9, suppressing the phospho-STAT3 (Tyr 705) and downregulating anti-apoptotic proteins like Bcl-2/Bcl-xL. Moreover, migration and invasion abilities of HCC cells were also inhibited by EH-42 in the wound healing assay and transwell invasion assay. The potential mechanism was that EH-42 could inhibit HCC metastasis via reversing epithelial-mesenchymal transition and downregulating the secretion of MMPs.
Frontiers in Clinical Drug Research – Anti-Cancer Agents brings updated and critical information about developing clinical trials and research in anti-cancer research. Reviews in each volume are written by experts in medical oncology and clinical trials research and compile the latest information available on special topics of interest to oncology researchers.
The fifth volume of the series features reviews on biochemical inhibitors (second-generation protein kinase Inhibitors, histone deacetylase inhibitors, immune checkpoint inhibitors, EGFR Tyrosine Kinase inhibitors, non-coding RNAs), apoptosis, and physical exercise therapy for cancer patients undergoing chemotherapy. The treatment strategies in this volume cover neoplasms such as acute myeloid leukemia, gastrointestinal cancer, breast cancer and lung cancer. Read full press release to find out more at: https://www.eurekalert.org/pub_releases/2019-06/bsp-fic062019.php
Aging has serious consequences on skeletal muscle. ‘Sarcopenia’, the progressive loss of muscle mass and associated muscle weakness during elderly, affects radically the functional capacity and general health in adult people and renders frail elders susceptible to serious injury from sudden falls and fractures and at risk for losing their functional independence. There is a vital need to recognise the molecular mechanisms and regulatory factors, underlying age-related muscle wasting and to develop therapeutic strategies that can attenuate, prevent, or finally reverse sarcopenia. In this context, sexual hormones play a key role.
The book, SEX STEROIDS AND APOPTOSIS IN SKELETAL MUSCLE: MOLECULAR MECHANISMS, written by Dr. Andrea Vasconsuelo aims to provide a new way to perceive the role of sex hormones in skeletal muscle. The book present in integrated form the latest information on sarcopenia and its relation with apoptosis, from leading researchers studying the cellular and molecular mechanisms underlying age-linked changes in skeletal muscle emphasising on the role of satellite cells. The authors succeed to explain, how hormones are involved in muscle homeostasis and in the regulation of apoptosis process and how these two functions connect to maintain a healthy muscle or to trigger pathologies. Therefore, the goal of this work is the combination of that information focusing on the molecular level and resulting in the clarification of molecular mechanisms implicated in skeletal muscle aging; when apoptosis is more intense and sex hormones levels decline. Very interesting, the book contains a chapter describing molecular structure of phytoestrogens and their action on sex steroids receptors. In addition, it is possible to emphasize the drafting writing promoting easy and pleasant reading, numerous and careful documentation, high quality images of the authors’ experiments and comprehensive and updated bibliography. This ebook is of interest to graduates and postgraduates in the fields of medicine and biochemistry, researchers of different aspects of ageing biology and people of the pharmaceutical, and health-care industry. Read out the full version here.
The book series offers readers an insight into current and future therapeutic approaches for the prevention of different types of cancers, synthesizing new anti-cancer agents, new patented compounds, targets and agents for cancer therapy as well as recent molecular and gene therapy research.
The topics covered in the seventh volume of this series include:
– The role of inflammation in chemotherapy-induced neuromuscular effects
– Advances in nutrigenomics and relevant anti-cancer patents
– Stimuli-responsive nanocarriers for on-demand anti-cancer drug release
– Harnessing biochemical mechanisms that control autophagy for treating esophageal cancer
This article by Dr. Emine Sekerdag et al. is published in Current Neuropharmacology, Volume 16, Issue 9, 2018
The blood circulation to neurons is affected due to Ischemic, hemorrhagic stroke and subarachnoid hemorrhage stimulation the activation of pathophysiological responses i.e. mitochondrial death pathways, protein misfolding, apoptosis, pyroptosis, necrosis, autophagy, mitophagy, ferritinophagy, excitotoxicity, free radicals release, and inflammation. The review focuses on the recent updates in our knowledge about cellular death mechanisms caused by the loss of neuronal cells and astrocytes, damage to white matter.
Novel treatment preferences in stroke involves restoration of blood flow control and the applicability of treatments is restricted due to a limited bioactive time window of thrombolytic agents. Ischemic, hemorrhagic stroke and subarachnoid hemorrhage are discussed in this review in relation to novel molecular, cellular treatment alternatives and cellular death mechanisms.