The polysaccharide from purple sweet potato ( Ipomoea batatas (L.) Lam) alleviates lipopolysaccharide-induced acute lung injury in mice via the VIP/ cAMP/PKA/AQPs signaling pathway

被引:0
|
作者
Yue, Maokui [1 ]
Shang, Wenli [2 ]
Zhang, Junli [1 ]
Chen, Ran [3 ]
Wei, Li [3 ]
Wang, Haidong [4 ]
Meng, Meng [5 ]
Zhang, Min [1 ]
Liu, Qinghua [6 ]
机构
[1] Shandong First Med Univ, Affiliated Hosp 2, Emergency Med, 366 Taishan Rd, Tai An 271000, Peoples R China
[2] Shandong First Med Univ, Affiliated Hosp 2, Dept Crit Care Med, 366 Taishan Rd, Tai An 271000, Peoples R China
[3] Shandong First Med Univ, Affiliated Hosp 2, Pulm & Crit Care Med, 366 Taishan Rd, Tai An 271000, Peoples R China
[4] Shandong First Med Univ, 2 Yingsheng East Rd, Tai An 271000, Peoples R China
[5] Coll Food Sci & Engn, State Key Lab Food Nutr & Safety, Key Lab Food Nutr & Safety, Minist Educ, Tai An, Peoples R China
[6] Shandong First Med Univ, Affiliated Hosp 2, Dept Clin Lab, 366 Taishan Rd, Tai An 271000, Peoples R China
关键词
Purple sweet potato; Polysaccharide; Acute lung injury; VIP/cAMP/PKA/AQPs; Immunity regulation; EXPRESSION; ANTHOCYANINS; ACTIVATION; MODEL;
D O I
10.1016/j.ijbiomac.2024.137428
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Background: The polysaccharide (PSP) from purple sweet potato has great potential for regulating apoptosis, but its regulatory role in acute lung injury (ALI) is unknown. Methods: The objective of this study was to investigate the protective effect of PSP on lipopolysaccharide (LPS)induced ALI in mice and lung epithelial A549 cells and its mechanism. Moreover, subacute toxicity evaluation of PSP was carried out on ICR mice. Results: The results showed that compared with the ALI group, PSP significantly reduced the total protein content, wet-to-dry (W/D) ratio, the number of neutrophils, lymphocytes, and monocytes. Moreover, PSP was able to reduce cell apoptosis, the levels of macrophage inflammatory protein-2 (MIP-2), intercellular adhesion molecule- 1 (ICAM-1), tumor necrosis factor-alpha (TNF-alpha), malondialdehyde (MDA) and myeloperoxidase (MPO) and increase the level of superoxide (SOD). In addition, PSP could up-regulate the levels of VIP, cAMP, p-PKA/PKA and AQP1 in mice and A549 cells. And PSP exhibited no apparent adverse effects on the mice. Conclusions: PSP had a protective effect on LPS-induced ALI in mice and lung epithelial A549 cells, which may be related to the inflammatory response and via VIP/cAMP/PKA/AQPs signaling pathway. Thus, PSP may be a promising pharmacologic agent for ALI therapy.
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页数:20
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