Neuroprotective effect of phospholipase A2 from Malaysian Naja sumatrana venom against H2O2-induced cell damage and apoptosis.

Oxidative stress is one of the factors involved in the pathogenesis of several neurodegenerative diseases. It has been reported that a secretory phospholipase A2 known as A2-EPTX-NSm1a has lower cytotoxicity in neuronal cells compared to its crude Naja sumatrana venom. In this study, A2-EPTX-NSm1a was tested for its neuroprotective activity on human neuroblastoma cells (SH-SY5Y) differentiated into cholinergic neurons against oxidative stress induced by hydrogen peroxide (H2O2). H2O2 treatment alone increased the caspase-3 and caspase-8 activities, whereas pre-treatment with A2-EPTX-NSm1a reduced the activity of these apoptosis-associated proteins. Moreover, A2-EPTX-NSm1a protects the morphology and ultrastructure of differentiated SH-SY5Y cells in the presence of H2O2. Oxidative stress increased the number of small mitochondria. Further evaluation showed the size of mitochondria with a length below 0.25 µm in oxidative stress conditions is higher than the control group, suggesting mitochondria fragmentation. Pre-treatment with A2-EPTX-NSm1a attenuated the number of mitochondria in cells with H2O2 Furthermore, A2-EPTX-NSm1a altered the expression of several neuroprotein biomarkers of GDNF, IL-8, MCP-1, TIMP-1, and TNF-R1 in cells under oxidative stress induced by H2O2. These findings indicate that anti-apoptosis with mitochondria-related protection, anti-inflammatory effect, and promote expression of important markers for cell survival may underlie the neuroprotective effect of A2-EPTX-NSm1a in cholinergic rich human cells under oxidative stress, a vital role in the neuronal disorder.

Cardioprotective Effects of Honey and Its Constituent: An Evidence-Based Review of Laboratory Studies and Clinical Trials.

Cardiovascular disease is a major public health burden worldwide. Myocardial infarction is the most common form of cardiovascular disease resulting from low blood supply to the heart. It can lead to further complications such as cardiac arrhythmia, toxic metabolite accumulation, and permanently infarcted areas. Honey is one of the most prized medicinal remedies used since ancient times. There is evidence that indicates honey can function as a cardioprotective agent in cardiovascular diseases. The present review compiles and discusses the available evidence on the effect of honey on cardiovascular diseases. Three electronic databases, namely, PubMed, Scopus, and MEDLINE via EBSCOhost, were searched between January 1959 and March 2020 to identify reports on the cardioprotective effect of honey. Based on the pre-set eligibility criteria, 25 qualified articles were selected and discussed in this review. Honey investigated in the studies included varieties according to their geological origin. Honey protects the heart via lipid metabolism improvement, antioxidative activity, blood pressure modulation, heartbeat restoration, myocardial infarct area reduction, antiaging properties, and cell apoptosis attenuation. This review establishes honey as a potential candidate to be explored further as a natural and dietary alternative to the management of cardiovascular disease.

Osteogenic Induction of Wharton's Jelly-Derived Mesenchymal Stem Cell for Bone Regeneration: A Systematic Review.

Wharton's jelly-derived mesenchymal stem cells (WJ-MSCs) are emerging as a promising source for bone regeneration in the treatment of bone defects. Previous studies have reported the ability of WJ-MSCs to be induced into the osteogenic lineage. The purpose of this review was to systematically assess the potential of WJ-MSC differentiation into the osteogenic lineage. A comprehensive search was conducted in Medline via Ebscohost and Scopus, where relevant studies published between 1961 and 2018 were selected. The main inclusion criteria were that articles must be primary studies published in English evaluating osteogenic induction of WJ-MSCs. The literature search identified 92 related articles, but only 18 articles met the inclusion criteria. These include two animal studies, three articles containing both in vitro and in vivo assessments, and 13 articles on in vitro studies, all of which are discussed in this review. There were two types of osteogenic induction used in these studies, either chemical or physical. The studies demonstrate that WJ-MSCs are able to differentiate into osteogenic lineage and promote osteogenesis. In light of these observations, it is suggested that WJ-MSCs can be a potential source of stem cells for osteogenic induction, as an alternative to bone marrow-derived mesenchymal stem cells.

The potential of Olea europaea extracts to prevent TGFß1-induced epithelial to mesenchymal transition in human nasal respiratory epithelial cells.

BACKGROUND: One of the molecular mechanisms involved in upper airway-related diseases is epithelial-to-mesenchymal transition (EMT). Olea europaea (OE) has anti-inflammatory properties and thus, great potential to prevent EMT. This study aimed to investigate the effect of OE on EMT in primary nasal human respiratory epithelial cells (RECs). METHODS: Respiratory epithelial cells were isolated and divided into four groups: control (untreated), treated with 0.05% OE (OE group), EMT induced with 5 ng/ml of transforming growth factor beta-1 (TGFß1 group) and treated with 5 ng/ml TGFß1 + 0.05% OE (TGFß1 + OE group). The effects of OE treatment on growth kinetics, morphology and protein expression in RECs were evaluated. Immunocytochemistry analysis was performed to quantitate the total percentage of E-cadherin and vimentin expression from day 1 to day 3. RESULTS: There were no significant differences between untreated RECs and OE-treated RECs in terms of their morphology, growth kinetics and protein expression. Induction with TGFß1 caused RECs to have an elongated spindle shape, a slower proliferation rate, a higher expression of vimentin and a lower expression of E-cadherin compared with the control. Cells in the TGFß1 + OE group had similar epithelial shape to untreated group however it had no significant differences in their proliferation rate when compared to TGFß1-induced RECs. Cells treated with TGFß1 + OE showed significantly reduced expression of vimentin and increased expression of E-cadherin compared with the TGFß1 group (P < 0.05). CONCLUSION: The ability of OE to inhibit EMT in RECs was shown by TGFb1-induced EMT REC morphology, growth kinetics and protein expression markers (E-cadherin and vimentin) upon treatment with OE and TGFß1. Therefore, this study could provide insight into the therapeutic potential of OE to inhibit pathological tissue remodelling and persistent inflammation.