Luteolin Relieved DSS-Induced Colitis in Mice via HMGB1-TLR-NF-κB Signaling Pathway

Zuo, Tao; Yue, Yinzi; Wang, Xiaohui; Li, Huan; Yan, Shuai

doi:10.1007/s10753-020-01354-2

Cited by 39 publications

(19 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Two cross-talking pathways are involved: Nrf2/HO-1 and the Toll-like receptor (TLR)/NF-κB axis [241]. Indeed, HMGB1 can suppress the Nrf2 pathway [236,242], as well as activating TLR-4, and thus activates NF-κB signaling [243,244]. Considering its crucial role in SOD induction, the Nrf2 pathway is an attractive target for different chronic diseases in which oxidative stress is involved [245,246].…”

Section: Sod As a Pharmacological Agentmentioning

confidence: 99%

Superoxide Dismutase Administration: A Review of Proposed Human Uses

et al. 2021

View full text Add to dashboard Cite

Superoxide dismutases (SODs) are metalloenzymes that play a major role in antioxidant defense against oxidative stress in the body. SOD supplementation may therefore trigger the endogenous antioxidant machinery for the neutralization of free-radical excess and be used in a variety of pathological settings. This paper aimed to provide an extensive review of the possible uses of SODs in a range of pathological settings, as well as describe the current pitfalls and the delivery strategies that are in development to solve bioavailability issues. We carried out a PubMed query, using the keywords “SOD”, “SOD mimetics”, “SOD supplementation”, which included papers published in the English language, between 2012 and 2020, on the potential therapeutic applications of SODs, including detoxification strategies. As highlighted in this paper, it can be argued that the generic antioxidant effects of SODs are beneficial under all tested conditions, from ocular and cardiovascular diseases to neurodegenerative disorders and metabolic diseases, including diabetes and its complications and obesity. However, it must be underlined that clinical evidence for its efficacy is limited and consequently, this efficacy is currently far from being demonstrated.

show abstract

Section: Sod As a Pharmacological Agentmentioning

confidence: 99%

Superoxide Dismutase Administration: A Review of Proposed Human Uses

et al. 2021

View full text Add to dashboard Cite

show abstract

“…All mice were weighed before anesthesia, and the entire colons were rapidly collected. e total colon lengths and weights were measured [26], and the colon weight index (CWI), CWI � colon weight/ body weight × 100%, was calculated [27,28]. Distal colon tissue was taken for pathological tissue testing.…”

Section: Histological Evaluationmentioning

confidence: 99%

Curcumin Alleviated Dextran Sulfate Sodium-Induced Colitis by Regulating M1/M2 Macrophage Polarization and TLRs Signaling Pathway

Kang

Wang

et al. 2021

Evidence-Based Complementary and Alternative Medicine

View full text Add to dashboard Cite

Curcumin has shown good efficacy in mice with experimental colitis and in patients with ulcerative colitis, but the mechanism of action through the regulation of M1/M2 macrophage polarization has not been elaborated. The ulcerative colitis was modeled by dextran sulfate sodium; colitis mice were orally administrated with curcumin (10 mg/kg/day) or 5-ASA (300 mg/kg/day) for 14 consecutive days. After curcumin treatment, the body weight, colon weight and length, colonic weight index, and histopathological damage in colitis mice were effectively improved. The concentrations of proinflammatory cytokines IL-1β, IL-6, and CCL-2 in the colonic tissues of colitis mice decreased significantly, while anti-inflammatory cytokines IL-33 and IL-10 increased significantly. Importantly, macrophage activation was suppressed and M1/M2 macrophage polarization was regulated in colitis mice, and the percentage of CD11b+F4/80+ and CD11b+F4/80+TIM-1+ and CD11b+F4/80+iNOS+ decreased significantly and CD11b+F4/80+CD206+ and CD11b+F4/80+CD163+ increased significantly. Additionally, curcumin significantly downregulated CD11b+F4/80+TLR4+ macrophages and the protein levels of TLR2, TLR4, MyD88, NF-κBp65, p38MAPK, and AP-1 in colitis mice. Our study suggested that curcumin exerted therapeutic effects in colitis mice by regulating the balance of M1/M2 macrophage polarization and TLRs signaling pathway.

show abstract

“…Studies showed that glycyrrhizin treatment suppressed IL-1β-induced NF-κB phosphorylation in a mouse model of osteoarthritis (OA), significantly reducing IL-6, prostaglandin E2 (PGE2), nitric oxide (NO) and TNF-α levels [ 34 ]. Additionally, luteolin decreased the levels of cytokines in mice serum and intestine by inhibiting the activation of NF-κB, relieving DSS-induced colitis [ 35 ]. In order to further explore whether the anti-inflammatory effect of neoastilbin is related to activation of the NF-κB pathway, a more in-depth study was conducted.…”

Section: Discussionmentioning

confidence: 99%

The Protective Effects of Neoastilbin on Monosodium Urate Stimulated THP-1-Derived Macrophages and Gouty Arthritis in Mice through NF-κB and NLRP3 Inflammasome Pathways

Zhang

et al. 2022

Molecules

View full text Add to dashboard Cite

Gouty arthritis (GA) is a frequent inflammatory disease characterized by pain, swelling, and stiffness of joints. Neoastilbin is a flavonoid isolated from the rhizome of Smilax glabra, which possesses various anti-inflammatory effects. However, the mechanism of neoastilbin in treating GA has not yet been clarified. Thus, this study was to investigate the protective effects of neoastilbin in both monosodium urate (MSU) stimulated THP-1-derived macrophages and the animal model of GA by injecting MSU into the ankle joints of mice. The levels of key inflammatory cytokines in MSU stimulated THP-1-derived macrophages were detected by enzyme-linked immunosorbent assay (ELISA) kits. Protein expressions of nuclear factor kappa B (NF-κB) and NOD-like receptor protein 3 (NLRP3) inflammasome pathways were further detected by Western blotting. In addition, swelling degree of ankle joints, the levels of inflammatory factors, infiltration of inflammatory cells and the expressions of related proteins were determined. Swelling degree and histopathological injury in ankle joints of MSU-injected mice were significantly decreased after being treated with neoastilbin. Moreover, neoastilbin significantly diminished the secretion of interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), suppressing the activation of NF-κB and NLRP3 inflammasome pathways in both MSU stimulated THP-1-derived macrophages and the mouse model of GA. In summary, neoastilbin could alleviate GA by inhibiting the NF-κB and NLRP3 inflammasome pathways, which provided some evidence for neoastilbin as a promising therapeutic agent for GA treatment.

show abstract

Luteolin Relieved DSS-Induced Colitis in Mice via HMGB1-TLR-NF-κB Signaling Pathway

Cited by 39 publications

References 12 publications

Superoxide Dismutase Administration: A Review of Proposed Human Uses

Superoxide Dismutase Administration: A Review of Proposed Human Uses

Curcumin Alleviated Dextran Sulfate Sodium-Induced Colitis by Regulating M1/M2 Macrophage Polarization and TLRs Signaling Pathway

The Protective Effects of Neoastilbin on Monosodium Urate Stimulated THP-1-Derived Macrophages and Gouty Arthritis in Mice through NF-κB and NLRP3 Inflammasome Pathways

Contact Info

Product

Resources

About