Oxidative stress plays a critical role in numerous diseases. Therefore, the pursuit of compounds with antioxidant activity remains critical. Green barley young leaves aqueous extract (GB) was tested for its capacity to ameliorate cellular oxidative stress, and its potential cytoprotective mechanism was partially elucidated. Through Folin-Ciocalteau and 1,1-diphenyl-2-picrylhydrazyl (DPPH) colorimetric assays, GB total phenolic content and free radical scavenging activity were found to be 59.91 ± 2.17 mg/L and 110.75 µg/ml (IC 50 ), respectively. Using a live cell-based propidium iodide dye exclusion assay and flow cytometry, GB was found to display significant cytoprotection activity on three human lymphocytic cell lines exposed to an aggressive H 2 O 2 -induced oxidative stress. The molecular mechanism for GB cytoprotection activity was assessed via bead-based xMAP technology on the Luminex platform and western blot analysis. GB treatment resulted in activation of Lyn, Akt, and ERK1/2, suggesting that GB is able to mitigate the H 2 O 2 -induced oxidative stress via activation of both the Lyn/PI3K/Akt and ERK/MAPK pathways. Our findings support the notion that GB extract has the potential to be a valuable therapeutic agent and may serve to establish a strategy to discover potential compound(s) or biological extracts/mixtures to be incorporated as a treatment to prevent oxidative stress-related diseases.
Background: IL-2 signaling occurs by cognate receptor phosphorylation, ultimately resulting in regulation of lymphocyte function. Results: IL-2R Thr(P)-450 positively regulates receptor complex stability and downstream STAT5 transcriptional activity. Conclusion: IL-2R Thr-450 is a novel ERK1/2-mediated phosphoregulatory site important for optimal IL-2 signal transduction. Significance: IL-2R threonine phosphorylation governs IL-2 signal transduction and may play a role in immune cell dysfunction.
Innate lymphoid cells (ILCs) are the most recently described group of lymphoid subpopulations. These tissue-resident cells display a heterogeneity resembling that observed on different groups of T cells, hence their categorization as cytotoxic NK cells and helper ILCs type 1, 2 and 3. Each one of these groups is highly diverse and expresses different markers in a context-dependent manner. Type 2 innate lymphoid cells (ILC2s) are activated in response to helminth parasites and regulate the immune response. They are involved in the etiology of diseases associated with allergic responses as well as in the maintenance of tissue homeostasis. Markers associated with their identification differ depending on the tissue and model used, making the study and understanding of these cells a cumbersome task. This review compiles evidence for the heterogeneity of ILC2s as well as discussion and analyses of molecular markers associated with their identity, function, tissue-dependent expression, and how these markers contribute to the interaction of ILC2s with specific microenvironments to maintain homeostasis or respond to pathogenic challenges.
Regulation of intracellular signaling pathways in lymphocytes is critical for cell homeostasis and immune response. Interleukin-2 (IL-2), a key regulator of lymphocytes, signals following receptor-ligand engagement and subsequent recruitment and activation of effector proteins including JAKs and STATs. Lymphocytes can also be regulated by the central nervous system through the β2 adrenergic receptor (β2AR) pathway which can affect cell trafficking, proliferation, differentiation, and cytokine production. The cross-talk between these two signaling pathways represents an important mechanism that has yet to be fully elucidated. The present study provides evidence for communication between the IL-2 receptor (IL-2R) and β2AR. Treatment of human lymphoid cell lines with the β2AR agonist isoproterenol (ISO) alone increased cAMP levels and mediated a stimulatory response by activating AKT and ERK to promote cell viability. Interestingly, ISO activation of β2AR also induced threonine phosphorylation of the IL-2Rβ. In contrast, ISO treatment prior to IL-2 stimulation produced an inhibitory signal that disrupted IL-2 induced activation of the JAK/STAT, MEK/ERK, and PI3K pathways by inhibiting the formation of the IL-2R beta–gamma chain complex, and subsequently cell proliferation. Moreover, γc-family cytokines-mediated STAT5 activation was also inhibited by ISO. These results suggest a molecular mechanism by which β2AR signaling can both stimulate and suppress lymphocyte responses and thus explain how certain therapeutic agents, such as vasodilators, may impact immune responsiveness.
The COVID-19 pandemic is responsible for millions of deaths worldwide yet its origin remains unclear. Two potential scenarios of how infection of humans initially occurred include zoonotic transfer from wild animals and a leak of the pathogen from a research laboratory. The Wuhan wet markets where wild animals are sold represent a strong scenario for zoonotic transfer. However, isolation of SARS-CoV-2 or its immediate predecessor from wild animals in their natural environment has yet to be documented.Due to incomplete evidence for a zoonotic origin, a laboratory origin is plausible. The Wuhan Institute of Virology is at the epicenter of the pandemic and their work has included manipulation of wild-type coronavirus to enable infection of human cells.Although stronger evidence supports the zoonotic transfer, inconclusive reports maintain the laboratory leak hypothesis alive. It is imperative to reach a factual conclusion to prevent future pandemics.
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