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Structural characterization and protective effects of polysaccharide from Gracilaria lemaneiformis on LPS-induced injury in IEC-6 cells

ABSTRACT: Highlights • GLP-1.6M was a sulfated red alga polysaccharide with a conformation of curved chains.• GLP-1.6M significantly inhibited the production of NO, TNF-α, IL-6 and IL-1β.• GLP-1.6M inhibited the expression of iNOS, TNF-α, IL-6, IL-1β and TLR-4.• GLP-1.6M promoted the expression of MUC-2, ZO-1, Occludin and Claudin-1. This study was aimed to characterize Gracilaria lemaneiformis polysaccharides and evaluate their protective effects on Lipopolysaccharide-induced injury in IEC-6 cells. The G. lemaneiformis polysaccharide was degraded by UV/H2O2 treatment and purified to three fractions named GLP-1.0 M, GLP-1.4 M and GLP-1.6 M. The purified fractions were mainly composed of galactose, glucose and xylose. The structural analysis showed that GLP-1.6 M was a typical sulfated red alga polysaccharide containing the linear backbone of β-(1 → 3)- and α-(1 → 4)-linked galactosyl residues, anhydro-galactose units. In the Lipopolysaccharide-induced IEC-6 cells model, GLP-1.6 M exerted the strongest in vitro anti-inflammatory activity by inhibiting the release and expressions of tumor necrosis factor-α, interleukin-6 and interleukin-1β by 89.93%, 67.82% and 38.06%, respectively. Meanwhile, GLP-1.6 M enhanced the intestinal barrier function via up-regulating the expressions of tight junctions and mucin. Therefore, the purified polysaccharide from G. lemaneiformis could be a promising candidate for maintaining intestinal health in the food and pharmaceutical industries.

SUBMITTER: Li X

PROVIDER: S-EPMC8593598 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Aim: Melatonin is an indolamine secreted by the pineal gland, as well as most of the organs and tissues. In addition to regulating circadian biology, studies have confirmed the multiple pharmacological effects of melatonin. Melatonin provides a strong defense against septic myocardial injury. However, the underlying mechanism has not been fully described. In this study, we investigated the protective effects of melatonin against lipopolysaccharide (LPS)-induced myocardial injury as well as the mechanisms involved. Methods: Mice were intraperitoneally injected with LPS to induce a septic myocardial injury model or an LPS shock model, depending on the dose of LPS. Melatonin was given (20 mg/kg/day, via intraperitoneal injection) for a week prior to LPS insult. 6 h after LPS injection, echocardiographic analysis, TUNEL staining, transmission electron microscopy (TEM), western blot, quantitative real-time PCR and ELISA were used to investigate the protective effects of melatonin against LPS induced myocardial injury. AMPK inhibitor, autophagy activator and inhibitor, siRNAs were used for further validation. Results: Survival test showed that melatonin significantly increased the survival rate after LPS-induced shock. In the sepsis model, melatonin markedly ameliorated myocardial dysfunction, decreased the release of inflammatory cytokines, activated AMP-activated protein kinase (AMPK), improved mitochondrial function, and activated autophagy. To confirm whether the protection of melatonin was mediated by AMPK and autophagy, Compound C, an AMPK inhibitor; 3-MA, an autophagy inhibitor; and Rapamycin (Rapa), an autophagy activator, were used in this study. AMPK inhibition down-regulated autophagy, abolished protection of melatonin, as indicated by significantly decreased cardiac function, increased inflammation and damaged mitochondrial function. Furthermore, autophagy inhibition by 3-MA significantly impaired the protective effects of melatonin, whereas autophagy activation by Rapa reversed LPS + Compound C induced myocardial injury. In addition, in vitro studies further confirmed the protection of melatonin against LPS-induced myocardial injury and the mechanisms involving AMPK-mediated autophagy signaling. Conclusions: In summary, our results demonstrated that melatonin protects against LPS-induced septic myocardial injury by activating AMPK mediated autophagy pathway.

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Structural characterization and protective effects of polysaccharide from Gracilaria lemaneiformis on LPS-induced injury in IEC-6 cells

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