Spermidine Alleviated LPS-initiated Inflammation by Activating Nrf2 Signaling Pathway

Zeng, Tao; Zhang, Xiu-Ning; Guo, Fangfang; Meng, Fan-Ge

doi:10.1016/j.freeradbiomed.2020.10.220

Cited by 1 publication

(2 citation statements)

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“…Additionally, we also found spermidine inhibited TNF-α gene expression in the LPS-stimulated cells, which implied spermidine mitigates the LPS-induced inflammatory response by downregulating the expression of pro-inflammatory cytokines. In line with our results, other studies also suggested that spermidine inhibits the production of pro-inflammatory cytokines in LPS-stimulated RAW264.7 cells [35]. To our knowledge, this is the first study to indicate that spermidine plays an important role in regulating the immune response of IPEC-J2 cells.…”

Section: Discussionsupporting

confidence: 92%

“…Likewise, spermidine has been reported to downregulate the expression of chemokines IL-6 in LPSstimulated macrophages [33]. Previous studies have reported that polyamine depletion causes inflammation by rapidly activating the NF-κB pathway in IEC-6 cells [34], and spermidine could protect against LPS-induced inflammatory response by abrogating the activation of the NF-κB pathway [11,35]. Consistent with these results, our data suggested spermidine treatment significantly inhibited the phosphorylation of NF-κB in porcine enterocytes stimulated by DEGBG.…”

Section: Discussionmentioning

confidence: 98%

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Effects of Spermidine on Cell Proliferation, Migration, and Inflammatory Response in Porcine Enterocytes

Wei¹,

Cai²,

Zhao³

et al. 2022

Front. Biosci. (Landmark Ed)

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Background:Polyamines have been demonstrated to be beneficial to porcine intestinal development. Our previous study showed that putrescine mitigates intestinal atrophy in weanling piglets and suppresses inflammatory response in porcine intestinal epithelial cells, it is still unknown the role of spermidine in mediating putrescine function. Objective: The current study aimed to investigate the effect of spermidine on the proliferation, migration, and inflammatory response in porcine intestinal epithelial cells (IPEC-J2 cell line). Methods: The effects of spermidine on proliferation and migration of IPEC-J2 cells were measured. Difluoromethyl ornithine (DFMO) and diethylglyoxal bis (guanylhydrazone) (DEGBG) were used to block the production of putrescine and spermidine, respectively. A cell inflammation model was established with lipopolysaccharides (LPS) stimulation. Gene expression and protein abundance were determined by real-time quantitative PCR and western blotting, respectively. Result: Spermidine significantly enhanced cell proliferation in DFMO (or/and) DEGBG treated IPEC-J2 cells (p < 0.05). Pretreatment with putrescine restored cell growth inhibited by DFMO but did not prevent the decrease in cell proliferation caused by DEGBG (p > 0.05). Similarly, spermidine but not putrescine significantly elevated the rate of migration in DEGBG treated IPEC-J2 cells (p < 0.05). Spermidine deprivation by DEGBG dramatically enhanced mRNA abundance of pro-inflammatory cytokines IL-8, IL-6, and TNF-α (p < 0.05), and the addition of spermidine attenuated excessive expression of those inflammatory pro-inflammatory cytokines, moreover, spermidine but not putrescine suppressed the phosphorylation of NF-κB induced by DEGBG. Spermidine supplementation also significantly suppressed LPS-induced the expression of TNF-α. Conclusions: The present study highlights a novel insight that putrescine may be converted into spermidine to modulate cell proliferation, migration, and inflammatory response on porcine enterocytes.

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Section: Discussionsupporting

confidence: 92%