Abstract
Numerous herbal-derived natural products are excellent anti-inflammatory agents. Several studies have reported that aloin, the major anthraquinone glycoside obtained from the Aloe species, exhibits anti-inflammatory activity. However, the molecular mechanism of this activity is not well understood. In this report, we found that aloin suppresses lipopolysaccharide-induced pro-inflammatory cytokine secretion and nitric oxide production, and downregulates the expression of tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2). Aloin inhibits the phosphorylation and acetylation of the NF-κB p65 subunit by suppressing the upstream kinases p38 and Msk1, preventing LPS-induced p65 translocation to the nucleus. We have also shown that aloin inhibits LPS-induced caspase-3 activation and apoptotic cell death. Collectively, these findings suggest that aloin effectively suppresses the inflammatory response, primarily through the inhibition of NF-κB signaling.
Highlights
In response to infection or tissue injury, immune cells initiate signaling cascades that trigger the release of various pro-inflammatory cytokines to combat tissue injury or pathogen invasion.Macrophages play important roles in the initiation, maintenance, and resolution of inflammation.Macrophage dysfunction can cause a variety of human inflammatory disorders, such as microbial infection, sepsis-related multiple organ failure, tumorigenesis, cardiovascular and metabolic diseases, and autoimmune diseases.The transcription factor NF-κB plays a vital role in inflammatory and immune responses
Aloin, which is known as barbaloin, is the major anthraquinone glycoside obtained from the Aloe species
We show that aloin protects macrophages from a lipopolysaccharide cells
Summary
In response to infection or tissue injury, immune cells initiate signaling cascades that trigger the release of various pro-inflammatory cytokines to combat tissue injury or pathogen invasion.Macrophages play important roles in the initiation, maintenance, and resolution of inflammation.Macrophage dysfunction can cause a variety of human inflammatory disorders, such as microbial infection, sepsis-related multiple organ failure, tumorigenesis, cardiovascular and metabolic diseases, and autoimmune diseases.The transcription factor NF-κB plays a vital role in inflammatory and immune responses. In response to infection or tissue injury, immune cells initiate signaling cascades that trigger the release of various pro-inflammatory cytokines to combat tissue injury or pathogen invasion. Macrophages play important roles in the initiation, maintenance, and resolution of inflammation. The transcription factor NF-κB plays a vital role in inflammatory and immune responses. NF-κB is highly activated at sites of inflammation in many diseases, and can induce the transcription of pro-inflammatory cytokines and chemokines, as well as various target genes, including inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) [1,2,3]. The NF-κB complex contains sites for post-translational modifications, which are important for activation and crosstalk with other signaling pathways [1,7,8].
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