The venom of (v) poses a threat to human health, as it contains a mixture of toxins that can cause cytotoxic, necrotic, and hemolytic effects. The present study assessed methanolic and acetone extracts from leaves and flowers of , as well as the bark of as potential suppressors of the toxic effects of v. The content of total phenols, flavonoids, and tannins of the plant extracts were quantified for the suppression of v cytotoxicity in two cell culture models, human lymphocytes and porcine aortic endothelial (PAE) cells. Extracts from displayed a greater concentration of total phenols, flavonoids, and tannins. Co-incubation of lymphocytes and PAE cells with fixed concentrations of v and plant extracts resulted in decreased v-induced cytotoxicity. A 24-hour co-incubation of lymphocytes with v (2.36 ± 0.17 µg/mL) and 0.5 µg/mL of methanolic leaf extract from (LLM) significantly suppressed the venom-induced cytotoxicity by 37.33 ± 8.33%. Similarly, the LLM extract (4 µg/mL) caused a significant decrease in v cytotoxicity after 24 hours in PAE cells. In contrast, while the acetone extract of bark (QA) suppressed cytotoxicity by 29.20 ± 3.51% ( < 0.001) in lymphocytes, it failed to protect PAE cells against v after 24 hours. In PAE cells, a shorter 4-hour co-incubation showed significant suppression of cytotoxicity with both extracts. Our results collectively suggest that LLM and QA possess cytoprotective properties against the toxic effects of v, and thus establish extracts from these plants as potential therapeutic interventions against envenomation.
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http://dx.doi.org/10.1080/01480545.2020.1856864 | DOI Listing |
Sci Rep
December 2024
Department of Frontier Medicine, Institute of Medical Science, Graduate School of Medicine, St. Marianna University, Kawasaki, 2168511, Japan.
The overexpression of Polo-like kinase 1 (PLK1) is associated with poor clinical outcomes in various malignancies, making it an attractive target for anticancer therapies. Although recent studies suggest PLK1's involvement in homologous recombination (HR), the impact of its overexpression on HR remains unclear. In this study, we investigated the effect of PLK1 overexpression on HR using bioinformatics and experimental approaches.
View Article and Find Full Text PDFCells
November 2024
Department of Pediatrics, University of New Mexico School of Medicine, Albuquerque, NM 87131, USA.
Prenatal alcohol exposure (PAE) is associated with long-term neurodevelopmental deficits resulting in impaired executive functioning and motor control. Intriguingly, PAE has been linked with an increased risk of transient systemic hypoxia-ischemia (TSHI), which alone results in suboptimal fetal growth and neurodevelopmental consequences. Here, using two translationally relevant preclinical models, we investigated the short-term and lasting effects of PAE and TSHI on the morphology of the medial prefrontal cortex (mPFC), a region important in executive function, and tested whether PAE interacts with TSHI to produce a distinct pattern of injury relative to either condition alone.
View Article and Find Full Text PDFHeliyon
December 2024
Functional Biomaterial Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Jeongeup, 56212, Republic of Korea.
Ethnopharmacological Relevance: The pharmacological potential of marine organisms remains largely unexplored. commonly known as Pae, is extensively distributed over Asia. Its antioxidant, antibacterial, antiobesity, and anti-inflammatory properties are also being investigated.
View Article and Find Full Text PDFInt J Mol Sci
November 2024
Natural Product Research Center, Institute of Natural Products, Korea Institute of Science and Technology, Gangneung 25451, Republic of Korea.
Oxidative stress induced by glutamate is a significant contributor to neuronal cell damage and can lead to neurodegenerative diseases such as Alzheimer's, Huntington's, and ischemic brain injury. At the cellular level, oxidative stress increases Ca ion influx and reactive oxygen species (ROS), which activate the MAPK signaling pathway. Additionally, the generation of ROS causes mitochondrial dysfunction, triggering apoptosis by promoting the translocation of AIF to the nucleus from the mitochondria.
View Article and Find Full Text PDFNat Commun
November 2024
Department of Medicine, Division of HIV, Infectious Diseases & Global Medicine, University of California San Francisco, San Francisco, CA, USA.
Despite antiretroviral therapy (ART), HIV persists in latently-infected cells (the HIV reservoir) which decay slowly over time. Here, leveraging >500 longitudinal samples from 67 people living with HIV (PLWH) treated during acute infection, we developed a mathematical model to predict reservoir decay from peripheral CD4 + T cells. Nonlinear generalized additive models demonstrated rapid biphasic decay of intact DNA (week 0-5: t ~ 2.
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