Neuroprotective effects of some epigenetic modifying drugs’ on Chlamydia pneumoniae-induced neuroinflammation: A novel model

Abstract

Chlamydia pneumoniae (Cpn) is a gram-negative intracellular pathogen that causes a variety of pulmonary diseases, and there is growing evidence that it may play a role in Alzheimer’s disease (AD) pathogenesis. Cpn can interact functionally with host histones, altering the host’s epigenetic regulatory system by introducing bacterial products into the host tissue and inducing a persistent inflammatory response. Because Cpn is difficult to propagate, isolate, and detect, a modified LPS-like neuroinflammation model was established using lyophilized cell free supernatant (CFS) obtained from infected cell cultures, and the effects of CFS were compared to LPS. The neuroprotective effects of Trichostatin A (TSA), givinostat, and RG108, which are effective on epigenetic mechanisms, and the antibiotic rifampin, were studied in this newly introduced model and in the presence of amyloid beta (Aβ) 1–42. The neuroprotective effects of the drugs, as well as the effects of CFS and LPS, were evaluated in Aβ-induced neurotoxicity using a real-time cell analysis system, total ROS, and apoptotic impact. TSA, RG108, givinostat, and rifampin all demonstrated neuroprotective effects in both this novel model and Aβ-induced neurotoxicity. The findings are expected to provide early evidence on neuroprotective actions against Cpn-induced neuroinflammation and Aβ-induced neurotoxicity, which could represent a new treatment option for AD, for which there are currently few treatment options.

Methyl group donor reduces the Caffeine hippocampal anti-inflammatory effects and potentiates the LPS effect by positive transcription of the Nrf2/Txn1/Nlrp3 axis

“…Our results corroborate, at least in part, with data from the literature. The neuroprotective effect of the RG108 inhibitor observed here can be correlated with a recent study that also reported its neuroprotective effect in a murine model of beta-amyloid (Aβ)-induced neurotoxicity [41]. On the other hand, studies report that SAMe, in a dose dependent manner, protects hippocampal CA1 neurons from degeneration and necrosis in rats subjected to transient and brief forebrain ischemia [42] in addition to induces antidepressant effects in preclinical and clinical studies of depression [43].…”

Evaluation of Cell Proliferation and Wound Healing Effects of Vitamin A Palmitate-Loaded PLGA/Chitosan-Coated PLGA Nanoparticles: Preparation, Characterization, Release, and Release Kinetics

“…After 3 h, the medium was discarded, 100 μL of dimethyl sulfoxide (DMSO) was added to each well, and absorbance at 540 and 570 nm wavelengths were measured in a Cytation 3 multimode reader device (Biotek). The absorbance values obtained from the wells were correlated to the number of live cells, which was expressed as a percentage of the control group …”

“…The absorbance values obtained from the wells were correlated to the number of live cells, which was expressed as a percentage of the control group. 48 …”

“…The absorbance values obtained from the wells were correlated to the number of live cells, which was expressed as a percentage of the control group. 48 Determination of Wound Healing Effects of Nanoparticle Formulations. To elucidate the wound healing activity, an Oris Cell Migration Assay Kit (Platypus Technologies) was used.…”