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Marine Microbial Polysaccharides: Promising Immunomodulatory and Anticancer Potential
Published in Shakeel Ahmed, Aisverya Soundararajan, Marine Polysaccharides, 2018
Jing Li, Bingxiang Shen, Songliu Nie, Kaoshan Chen
Macrophages are derived from blood monocytes and play important roles in the host defense system against microbial infections and tumours [39]. Many studies reported that marine microbial polysaccharides can affect the functions of macrophages [40]. The effects of the Antarctic bacterium extracellular polysaccharide (PEP) on peritoneal macrophages were studied. Treatment with PEP can cause morphological alterations in macrophages, increase the endocytic index, cause a great increase in NO production and induce the secretion of tumour necrosis factor (TNF)-α and interleukin (IL)-1β. However, this polysaccharide does not affect respiratory burst. Further studies found that this activation was through nuclear factor kappa B (NF-кB) and p38 mitogen-activated protein kinase (MAPK) signalling pathways [29, 41]. The marine fungus polysaccharide YCP had a stimulatory effect on the production of NO in macrophages. Fluorescence-labelled YCP (fl-YCP) was prepared, and it was found that fl-YCP can bind to receptors on the surface of macrophages. In addition, competition studies showed that TLR4 and CR3 may be the receptors which YCP binds to. Furthermore, western blotting showed that YCP significantly activates p38 MAPK in a time-dependent manner and YCP-induced NO production is abrogated by p38 inhibitor, anti-TLR4 antibody and anti-CR3 antibody. These results indicated that YCP can activate macrophages through TLR4 and CR3 in a p38 kinase-dependent manner [42]. EPS (microalgal sulphated exopolysaccharide [MSE]) from the marine microalga Gyrodinium impudicum (strain KG03) induced murine peritoneal macrophages to show a cytotoxic effect on tumour cells, and the tumour cytotoxicity induced by MSE was partially abrogated by a NO inhibitor. Therefore, the tumouricidal activity induced by MSE may be attributed to the production of NO. In addition, with c-Jun N-terminal kinase (JNK) inhibitor treatment, electrophoretic mobility shift assay analyses revealed that the tumouricidal activity induced by MSE was mediated probably via the NF-κB and JNK pathways [43].
Protective effects of natural compounds against paraquat-induced pulmonary toxicity: the role of the Nrf2/ARE signaling pathway
Published in International Journal of Environmental Health Research, 2023
Hasan Badibostan, Nastaran Eizadi-Mood, A. Wallace Hayes, Gholamreza Karimi
Xuebijing injection is a Chinese herbal medicine consisting of a mixture of Chuanxiong, Chishao, Danshen, and Honghua (Liu et al. 2014). PQ increased MAPK expression and stimulated the production of TNF-α and IL-1β in the lungs of rats (Liu et al. 2014). p38 Mitogen-activated protein kinases (MAPK) are key mediators of cellular stressors such as inflammatory cytokines. MAPK indirectly decreased the Nrf2 level (Liu et al. 2014). Liu et al. investigated the protective effect of Xuebijing in an animal model. Their findings suggested that this herbal mixture decreased IL-6, TNF-α, IL-1β, IL-10, and TGF-β1 levels in PQ-treated animals. Although the levels of Nrf2 and GSH were increased in the lungs, Xuebijing was reported to protect rats against PQ lung-induced toxicity through the down-regulation of MAPK (Liu et al. 2014).