• Biomedical Science Letters
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• v.28 no.4
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• pp.276-283
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• 2022

Saccharina japonica (SJ), a brown algae, exerts various pharmacological effects, including anti-oxidant, immunemodulating and anti-cancer properties. This study aimed to determine the pharmacological mechanism of SJ on atopic dermatitis in vivo and in vitro. We investigated the pharmacological effects of SJ on 2, 4-dinitrochlrobenzene (DNCB)- induced atopic dermatitis clinical symptoms in mice. Additionally, we evaluated the effects of SJ on the inflammatory cytokine production and nuclear factor-κB (NF-κB) activation in HaCaT cells. The findings of this study demonstrated that SJ reduced the clinical symptoms of atopic dermatitis, such as skin dryness, erythema and eczematous, and serum histamine and IgE level in DNCB-induced atopic dermatitis model. Additionally, SJ inhibited the NF-κB activation in atopic dermatitis-like skin lesion and HaCaT cells. Collectively, this result suggests that SJ could be used as a therapeutic agent for skin inflammation, including atopic dermatitis.

• Journal of Life Science
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• v.33 no.6
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• pp.463-470
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• 2023

Desmarestia tabacoides Okamura is a brown macroalgae that is found worldwide. Although several genera of Desmarestia have been reported as having anti-tumorigenic, anti-melanogenic, and photoprotective properties, the anti-inflammatory activity of D. tabacoides Okamura has not yet been evaluated. In this study, we analyzed the anti-inflammatory mechanisms of D. tabacoides Okamura ethanol extract (DTEE) via the inhibition of nitric oxide (NO) and prostaglandin (PG) E₂ production and the expression of their corresponding enzymes, inducible NO synthase (iNOS), and cyclooxygenase (COX)-2. In addition, their upstream signaling molecules were evaluated by Western blot analysis, such as nuclear factor (NF)-κB, mitogen-activated protein kinase (MAPK), and phosphoinositide-3-kinase (PI3K)/Akt, in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. The DTEE treatment significantly inhibited LPS-induced NO and PGE₂ production as well as the expression of their corresponding enzymes, iNOS, and COX-2 without cytotoxicity. The stimulated transcription factor NF-κB and upstream signaling molecules extracellular signal-regulated kinase (ERK), c-Jun NH₂-terminal kinase (JNK), and p38 were attenuated by the DTEE treatment, which was statistically significant, while Akt did not provide any inhibitory effect. Moreover, the DTEE treatment significantly mitigated the LPS-activated adaptor molecules, toll-like receptor 4 (TLR4), and myeloid differentiation primary response 88 (MyD88) in the RAW 264.7 cells. These results suggest that DTEE attenuates TLR4-mediated inflammatory responses by inhibiting NF-κB activation and suppressing MAPK phosphorylation in LPS-stimulated RAW 264.7 cells.

• Biomolecules & Therapeutics
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• v.29 no.6
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• pp.637-642
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• 2021

In this study, we investigated whether eriodictyol exerts an effect on the production and gene expression of MUC5AC mucin in human pulmonary epithelial NCI-H292 cells. The cells were pretreated with eriodictyol for 30 min and then stimulated with phorbol 12-myristate 13-acetate (PMA) for 24 h. The effect of eriodictyol on PMA-induced nuclear factor kappa B (NF-κB) signaling pathway was also investigated. Eriodictyol suppressed the MUC5AC mucin production and gene expression induced by PMA via suppression of inhibitory kappa Bα degradation and NF-κB p65 nuclear translocation. These results suggest that eriodictyol inhibits mucin gene expression and production in human airway epithelial cells via regulation of the NF-κB signaling pathway.

• Biomedical Science Letters
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• v.29 no.2
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• pp.58-65
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• 2023

Pu-erh tea, a popular and traditional Chinese tea, possesses various health-promoting effects, including inhibiting tumor cell progression and preventing type II diabetes and neurodegenerative disorders. However, the precise anti-inflammatory mechanisms are not well understood. In present study, we elucidated the anti-inflammatory mechanism of Pu-erh tea in lipopolysaccharide (LPS)-activated RAW264.7 cells. We explored the effects of Pu-erh tea on the levels of inflammatory-related genes, including inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2 and prostaglandin E₂ (PGE₂) in LPS-activated RAW264.7 cells. Moreover, we investigated its regulatory effects on nuclear factor-kappa B (NF)-κB and hypoxia-inducible-factor (HIF)-1α activation. The findings of this study demonstrated that Pu-erh tea inhibited the LPS-increased inflammatory cytokines and PGE₂ release, as well as COX-2 and iNOS expression. Moreover, we confirmed that the anti-inflammatory mechanism of Pu-erh tea occurs via the inhibition of NF-κB and HIF-1α activation. Conclusively, these findings provide experimental evidence that Pu-erh tea may be useful candidate in the treatment of inflammatory-related diseases.

• Korean Journal of Food Science and Technology
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• v.53 no.2
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• pp.154-159
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• 2021

Barringtonia augusta Kurz is a species of the genus Barringtonia. Although several studies have analyzed the biological activity of B. racemosa Roxb and B. acutangula, the anti-inflammatory and antioxidant effects of B. augusta extract (BKE) remain unclear. Therefore, in this study, we investigated the anti-inflammatory and antioxidant effects of BKE using lipopolysaccharide (LPS) and RAW 264.7. BKE suppressed LPS-induced nitric oxide (NO) and inducible NO synthase expression without affecting RAW 264.7 cell viability. Additionally, BKE showed 2,2-Diphenyl-1-picrylhydrazyl and 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) radical scavenging capacities and inhibited LPS-induced reactive oxygen species production in RAW 264.7 cells. BKE also suppressed LPS-induced phosphorylation of IκB kinase and nuclear factor kappa-B (NF-κB) and p65 translocation from the cytosol to the nucleus in RAW 264.7 cells. These results suggest that BKE is a possible novel material that exerts beneficial antioxidant and anti-inflammatory effects through the inhibition of NF-κB signaling pathways.

• Journal of Applied Biological Chemistry
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• v.66
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• pp.447-454
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• 2023

In the environment in which humans live, there are various antigens that invade the human body and interfere with humans leading a healthy life, so the immune system recognizes the antigen then removes them through a complex mechanism. Macrophages are widely distributed immune cells involved in the innate immune system, and produce various immune modulators such as inducible nitric oxide synthase-induced nitric oxide, cyclooxygenase-2 induced prostaglandin E2 and proinflammatory cytokines such as tumor necrosis factor-alpha. On the other hand, Protaetia brevitarsis seulensis larvae are a type of edible insect that have emerged as an alternative to the future food supply problem. The immuno-modulatory effect through the activation of murine macrophage RAW264.7 cell via mitogen-activated protein kinases (MAPKs)/nuclear factor-kappa B (NF-κB) signaling pathways has been reported. Based on this report, in this study, we confirmed how the expression of immune modulators induced by Protaetia brevitarsis seulensis larvae extracts in RAW264.7 cells was changed by treatment with pharmacological inhibitors of toll-like receptor 4 (TLR4), MAPKs and NF-κB signaling pathways. As a result, reduction of immune modulators was confirmed in the c-Jun N-terminal kinase (JNK) inhibitor treatment group and NF-κB inhibitor treatment group among the Protaetia brevitarsis seulensis larvae-treated RAW264.7 cell. Furthermore, in the TLR4 inhibitor-treated group, decreases in phosphorylation of JNK and NF-κB factors were confirmed in Protaetia brevitarsis seulensis larvae-treated RAW264.7 cell, as well as decreases in immune modulators. This results suggest that Protaetia brevitarsis seulensis larvae activates RAW264.7 cells by the engagement of TLR4-JNK/NF-κB signaling pathway.

• The Korean Journal of Physiology and Pharmacology
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• v.25 no.4
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• pp.321-331
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• 2021

Vancomycin, an antibiotic used occasionally as a last line of treatment for methicillin-resistant Staphylococcus aureus, is reportedly associated with nephrotoxicity. This study aimed at evaluating the protective effects of lutein against vancomycin-induced acute renal injury. Peroxisome proliferator-activated receptor gamma (PPARγ) and its associated role in renoprotection by lutein was also examined. Male BALB/c mice were divided into six treatment groups: control with normal saline, lutein (200 mg/kg), vancomycin (250 mg/kg), vancomycin (500 mg/kg), vancomycin (250 mg/kg) with lutein, and vancomycin (500 mg/kg) with lutein groups; they were euthanized after 7 days of treatment. Thereafter, samples of blood, urine, and kidney tissue of the mice were analyzed, followed by the determination of levels of N-acetyl-β-D-glucosaminidase (NAG) in the urine, renal creatine kinase; protein carbonyl, malondialdehyde, and caspase-3 in the kidney; and the expression of PPARγ, nuclear factor erythroid 2-related factor 2 (Nrf2), and nuclear factor-kappaB (NF-κB) in renal tissue. Results showed that the levels of protein carbonyl and malondialdehyde, and the activity of NAG, creatine kinase and caspase-3, were significantly increased in the vancomycin-treatment groups. Moreover, the levels of Nrf2 significantly decreased, while NF-κB expression increased. Lutein ameliorated these effects, and significantly increased PPARγ expression. Furthermore, it attenuated vancomycin-induced histological alterations such as, tissue necrosis and hypertrophy. Therefore, we conclude that lutein protects against vancomycin-induced renal injury by potentially upregulating PPARγ/Nrf2 expression in the renal tissues, and consequently downregulating the pathways: inflammation by NF-κB and apoptosis by caspase-3.

• Korean Journal of Plant Resources
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• v.36 no.6
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• pp.549-555
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• 2023

Hijikia fusiforme (HF), a member of brown algae family, exerts various pharmacological effects, including preventing arteriosclerosis and menopausal disorders. This study aimed to elucidate the ameliorative effect of HF on skin inflammation. We investigated the antioxidant and anti-inflammatory effect of HF extract to evaluate its potential as a functional materials. The antioxidant activity of HF was determined using 2,2-diphenyl-1-picrylhydrazy (DPPH) scavenging and 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS+) scavenging. To determine the pharmacological mechanism of HF in inflammatory reaction, we evaluated the effects of HF on interleukin (IL)-8, IL-6 and tumor necrosis factor (TNF)-α production and nuclear factor-κB (NF-κB) activation in activated- human mast cells (HMC)-1. Results showed that HF had the high DPPH and ABTS+ radical scavenging activity, and it suppressed IL-8, IL-6 and TNF-α production in a concentration-dependent manner. Moreover, HF significantly ameliorated NF-kB activation in activated-HMC-1. Hence, these results provide evidence that HF's potential for skin inflammation therapy.

• Biomolecules & Therapeutics
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• v.28 no.2
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• pp.152-162
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• 2020

Cerebral ischemia exhibits a multiplicity of pathophysiological mechanisms. During ischemic stroke, the reactive oxygen species (ROS) concentration rises to a peak during reperfusion, possibly underlying neuronal death. Recombinant human erythropoietin (EPO) supplementation is one method of treating neurodegenerative disease by reducing the generation of ROS. We investigated the therapeutic effect of PEGylated EPO (P-EPO) on ischemic stroke. Mice were administered P-EPO (5,000 U/kg) via intravenous injection, and middle cerebral artery occlusion (MCAO) followed by reperfusion was performed to induce in vivo ischemic stroke. P-EPO ameliorated MCAO-induced neurological deficit and reduced behavioral disorder and the infarct area. Moreover, lipid peroxidation, expression of inflammatory proteins (cyclooxygenase-2 and inducible nitric oxide synthase), and cytokine levels in blood were reduced by the P-EPO treatment. In addition, higher activation of nuclear factor kappa B (NF-κB) was found in the brain after MCAO, but NF-κB activation was reduced in the P-EPO-injected group. Treatment with the NF-κB inhibitor PS-1145 (5 mg/kg) abolished the P-EPO-induced reduction of infarct volume, neuronal death, neuroinflammation, and oxidative stress. Moreover, P-EPO was more effective than EPO (5,000 U/kg) and similar to a tissue plasminogen activator (10 mg/kg). An in vitro study revealed that P-EPO (25, 50, and 100 U/mL) treatment protected against rotenone (100 nM)-induced neuronal loss, neuroinflammation, oxidative stress, and NF-κB activity. These results indicate that the administration of P-EPO exerted neuroprotective effects on cerebral ischemia damage through anti-oxidant and anti-inflammatory properties by inhibiting NF-κB activation.

• Journal of Veterinary Science
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• v.21 no.3
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• pp.50.1-50.16
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• 2020

Background: Porcine parvovirus (PPV) is a single-stranded DNA virus that causes porcine reproductive failure. It is of critical importance to study PPV pathogenesis for the prevention and control of the disease. NS1, a PPV non-structural protein, is participated in viral DNA replication, transcriptional regulation, and cytotoxicity. Our previous research showed that PPV can activate nuclear factor kappa B (NF-κB) signaling pathway and then up-regulate the expression of interleukin (IL)-6. Objectives: Herein, the purpose of this study is to determine whether the non-structural protein NS1 of PPV also has the same function. Methods: Real-time quantitative reverse transcription polymerase chain reaction (RT-qPCR), enzyme-linked immunosorbent assay, western blot, immunofluorescence assay and small interfering RNA (siRNA) were used. Results: Our findings demonstrated that PPV NS1 protein can up-regulate the expression levels of IL-6 and tumor necrosis factor-alpha in a dose-dependent manner. Moreover, PPV NS1 protein was found to induce the phosphorylation of IκBα, then leading to the phosphorylation and nuclear translocation of NF-κB. In addition, the NS1 protein activated the upstream pathways of NF-κB. Meanwhile, TLR2-siRNA assay showed TLR2 plays an important role in the activation of NF-κB signaling pathway induced by PPV-NS1. Conclusions: These findings indicated that PPV NS1 protein induced the up-regulated of IL-6 expression through activating the TLR2 and NF-κB signaling pathways. In conclusion, these findings provide a new avenue to study the innate immune mechanism of PPV infection.