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Communication

2-Bromo-5-Hydroxy-4-Methoxybenzaldehyde Exhibits Anti-Inflammatory Effects Through the Inactivation of ERK, JNK, and NF-kB Pathways in RAW 264.7 Cells

by
Junseong Kim
1,
Seong-Yeong Heo
1,
Eun-A Kim
1,
Nalae Kang
1 and
Soo-Jin Heo
1,2,*
1
Jeju Marine Research Center, Korea Institute of Ocean Science and Technology (KIOST), Jeju 63349, Republic of Korea
2
Department of Biology, University of Science and Technology (UST), Daejeon 34113, Republic of Korea
*
Author to whom correspondence should be addressed.
Phycology 2026, 6(1), 10; https://doi.org/10.3390/phycology6010010
Submission received: 23 October 2025 / Revised: 19 December 2025 / Accepted: 4 January 2026 / Published: 7 January 2026
(This article belongs to the Special Issue Seaweed Metabolites)
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Abstract

Inflammation plays a central role in the pathogenesis of numerous diseases through the excessive production of nitric oxide (NO), prostaglandins, and pro-inflammatory cytokines. Although bromophenols from marine algae and various phenolic compounds exhibit strong anti-inflammatory activity, the biological properties of brominated vanillin derivatives remain largely unexplored. This study aimed to investigate the anti-inflammatory effects of 2-bromo-5-hydroxy-4-methoxybenzaldehyde (2B5H4M), a brominated vanillin derivative structurally similar to marine bromophenols, in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. 2B5H4M significantly reduced LPS-induced NO and PGE2 production by suppressing the protein and mRNA expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). It also downregulated the expression of pro-inflammatory cytokines, including TNF-α, IL-1β, and IL-6. Mechanistically, 2B5H4M inhibited the phosphorylation and degradation of IκB-α, thereby preventing NF-κB nuclear translocation, and reduced the phosphorylation of ERK and JNK. These findings demonstrate that 2B5H4M exerts potent anti-inflammatory effects by simultaneously blocking NF-κB and MAPK signaling pathways. Although not algae-derived, the structural resemblance of 2B5H4M to marine bromophenols highlights its potential as a marine-inspired reference compound. This work suggests that 2B5H4M may serve as a promising lead scaffold for developing new phenolic anti-inflammatory agents and provides a foundation for future mechanistic and in vivo studies.
Keywords:
inflammatory; ERK; JNK; RAW 264.7

1. Introduction

Inflammation has been widely recognized as a key factor in diseases, contributing significantly to conditions such as dermatitis, migraines, obesity, vascular diseases, and other serious health issues owing to the excessive production of inflammatory mediators [1,2,3]. These stimuli lead to the uncontrolled release of nitric oxide (NO), prostaglandins (PGs), and proinflammatory cytokines such as tumor necrosis factor-alpha, interleukin (IL)-1β, and IL-6, which can cause various disorders [4,5]. Macrophages, as pivotal inflammatory and immune effector cells, are activated in inflamed tissues upon exposure to various stimulators including interferon-g, tumor necrosis factor (TNF), and lipopolysaccharide (LPS) [6]. Exposure of macrophages to LPS initiates signaling pathways that culminate in the activation of mitogen-activated protein kinases (MAPKs) and nuclear factor-kappa B (NF-κB), ultimately leading to the production of key inflammatory mediators such as NO, PGE2, TNF-α, and IL-6 [7,8,9]. Several types of drugs, including biological, steroidal, and nonsteroidal anti-inflammatory drugs, are employed in the treatment of inflammatory disorders; yet, they are often associated with adverse side-effects, while in the case of biologics, treatment can be costly. Natural products provide an alternative avenue, holding promise for the identification of bioactive lead compounds, which may be further developed into drugs for the treatment of inflammatory disorders [10,11].
Phenolic compounds are secondary metabolites found in natural plants. Phenolic compounds, particularly simple phenols, have been reported as potent antioxidants, drawing considerable interest in recent years owing to their related health benefits. They exhibit various effects, including anticancer, antiviral, antibacterial, and anti-inflammatory activities. Among these, various simple phenolic esters such as caffeic acid, phenethyl, coumarin, and vanillin have been confirmed to possess anti-inflammatory effects [12,13,14,15]. Recent studies have demonstrated that phenolic acids and extracts attenuate LPS-induced macrophage inflammation through inhibition of NF-κB and MAPK signaling pathways in RAW 264.7 cells [16,17,18,19,20]. Marine algae are also rich in bioactive phenolics such as bromophenols and phlorotannins. Numerous seaweed-derived brominated compounds inhibit LPS-induced inflammation by regulating NF-κB or MAPK signaling. For example, red-algal bromophenols suppress ERK activation through ROS-mediated mechanisms [21], the phlorotannin 6,6′-bieckol from Ecklonia cava reduces NO/PGE2 and cytokines via NF-κB inhibition [22], and E. cava extracts attenuate TLR4–NF-κB/MAPK signaling in RAW 264.7 macrophages [23]. Recent reviews have emphasized that marine-derived phenolics, including phlorotannins and bromophenols, are increasingly recognized as promising modulators of macrophage-mediated inflammation [24,25,26]. These compounds have been shown to downregulate pro-inflammatory mediators by targeting NF-κB and MAPK signaling pathways, supporting the relevance of brominated phenolic scaffolds in inflammation research and highlighting the importance of continued investigation of marine-inspired phenolic structures.
The parent molecule vanillin has recently been shown to exert anti-inflammatory effects in macrophage and colitis models through suppression of TLR4 activation and NF-κB signaling [27,28,29]. However, most studies have focused on non-brominated phenolic aldehydes. Brominated vanillin derivatives such as BHMB and BVAN08 have been investigated mainly for anti-inflammatory or anticancer properties via MAPK or DNA-PKcs pathways [30,31]. Despite these findings, no study has systematically evaluated the anti-inflammatory effects of 2B5H4M in macrophages, leaving a clear knowledge gap in the understanding of brominated vanillin scaffolds.
Therefore, this study aimed to investigate the anti-inflammatory effects and underlying mechanisms of 2B5H4M in LPS-stimulated RAW 264.7 macrophages, and to determine whether this synthetic, non-algal brominated vanillin derivative can serve as a mechanistically relevant phenolic scaffold for inflammation-related research.

2. Materials and Methods

2.1. Materials

2-Bromo-5-hydroxy-4-methoxybenzaldehyde (2B5H4M, Figure 1), phosphate-buffered saline (PBS), and dimethyl sulfoxide (DMSO) were obtained from Sigma–Aldrich (St. Louis, MO, USA). Dulbecco’s Modified Eagle’s Medium (DMEM) and fetal bovine serum (FBS) were purchased from Gibco (Thermo Fisher Scientific, Grand Island, NY, USA). Antibodies specific for phosphorylated IκB-α (p-IκB-α), NF-κB (p65), JNK, phosphorylated JNK (p-JNK), ERK1/2, phosphorylated ERK1/2 (p-ERK1/2), p38, and phosphorylated p38 (p-p38) were supplied by Cell Signaling Technology (Beverly, MA, USA). Unless otherwise indicated, all other reagents were of analytical grade and purchased from Sigma–Aldrich.

2.2. Cell Culture

The murine macrophage cell line RAW 264.7 was obtained from the Korean Cell Line Bank (KCLB; Seoul, Republic of Korea). Cells were maintained in DMEM supplemented with 10% FBS, 100 U/mL penicillin, and 100 µg/mL streptomycin and incubated at 37 °C in a humidified atmosphere containing 5% CO2.

2.3. Measurement of Lactate Dehydrogenase (LDH) Cytotoxicity

RAW 264.7 macrophages (1.5 × 105 cells/mL) were cultured with lipopolysaccharide (LPS, 1 µg/mL) and various concentrations of 2B5H4M (37.5, 75, and 150 µM) at 37 °C for 24 h. After incubation, culture supernatants were collected and LDH release was measured using an LDH Cytotoxicity Detection Kit (Promega, Madison, WI, USA) following the manufacturer’s instructions. Briefly, 100 µL of reaction mixture was added to each well and incubated for 30 min at room temperature (25 °C) in the dark. Absorbance was read at 490 nm using a microplate reader (BioTek Instruments, Winooski, VT, USA).

2.4. Measurement of NO Production

For nitric oxide determination, RAW 264.7 cells (1.5 × 105 cells/mL) were treated with LPS (1 µg/mL) and 2B5H4M (37.5, 75, and 150 µM) for 24 h at 37 °C. Nitrite levels in the supernatants were quantified as an index of NO production using the Griess reaction. Equal volumes (100 µL) of culture supernatant and Griess reagent (1% sulfanilamide and 0.1% naphthylethylenediamine dihydrochloride in 2.5% phosphoric acid) were mixed and incubated for 10 min at 25 °C. Absorbance was measured at 540 nm, and nitrite concentrations were calculated from a sodium nitrite standard curve. Fresh medium served as a blank control.

2.5. Measurement of Cytokine Levels

DMSO-solubilized 2B5H4M was diluted with DMEM before use. RAW 264.7 cells were treated with LPS (1 μg/mL) in the presence or absence of 2B5H4M, and the inhibitory effect of 2B5H4M on the production of proinflammatory cytokines (TNF-α, IL-1β, and IL-6) was evaluated. The levels of proinflammatory cytokines in the culture supernatants were quantified using mouse ELISA kits (R&D Systems Inc., Minneapolis, MN, USA) according to the manufacturer’s instructions.

2.6. Reverse Transcriptase-PCR (RT-PCR) Analysis

Total RNA was extracted from treated RAW 264.7 cells using TRIzol reagent (Invitrogen, Carlsbad, CA, USA) according to the manufacturer’s instructions. One microgram of total RNA was reverse-transcribed into complementary DNA (cDNA) using M-MLV reverse transcriptase (Promega, Madison, WI, USA). PCR amplification was carried out using gene-specific primers. The primer sequences were as follows: COX-2 forward 5′-GGGGTACCTTCCAGCTGTCAAAATCTC-3′ and reverse 5′-GAAGATCTCGCCAGGTACTCACCTG-3′; iNOS forward 5′-CCCTTCCGAAGTTTCTGGCAGCAGC-3′ and reverse 5′-GGCTGTCAGAGCCTCGTGGCTTTGG-3′; IL-1β forward 5′-ATGGCAACTGTTCCTGAACTCAACT-3′ and reverse 5′-TTTCCTTTCTTAGATATGGACAGGAC-3′; IL-6 forward 5′-AGTTGCCTTCTTGGGACTGA-3′ and reverse 5′-CAGAATTGCCATTGCACAAC-3′; TNF-α forward 5′-ATGAGCACAGAAAGCATGATC-3′ and reverse 5′-TACAGGCTTGTCACTCGAATT-3′; and GAPDH forward 5′-TGAAGGTCGGTGTGAACGGATTTGGC-3′ and reverse 5′-CATGTAGGCCATGAGGTCCACCAC-3′. PCR products were separated by electrophoresis on agarose gels, and the resulting bands were visualized under ultraviolet illumination.

2.7. Western Blotting

Following treatment, RAW 264.7 cells were collected and lysed to obtain nuclear and cytoplasmic fractions using the NE-PER® Nuclear and Cytoplasmic Extraction Kit (Thermo Fisher Scientific, Waltham, MA, USA). Protein concentrations were measured with a BCA Protein Assay Kit (Thermo Fisher Scientific). Equal amounts of protein (30 µg) were resolved by 10% SDS-PAGE and transferred onto nitrocellulose membranes (Merck Millipore, Cork, Ireland). After blocking with 5% (w/v) skim milk in TBST, membranes were incubated with specific primary antibodies and then with HRP-conjugated secondary antibodies. Signals were detected using ECL reagents (Cyanagen Srl, Bologna, Italy) and visualized on a Davinch-Chemi™ imaging system (CoreBio, Seoul, Republic of Korea).

2.8. Statistical Analysis

All data are presented as the mean ± SD. Statistical significance among multiple groups was assessed using one-way ANOVA followed by Dunnett’s post hoc test. A p-value of <0.05 was considered statistically significant. All analyses were performed using GraphPad Prism (version 9, GraphPad Software, San Diego, CA, USA).

3. Results and Discussion

3.1. Cytotoxicity of 2B5H4M in RAW 264.7 Cells

The cytotoxic effect of 2B5H4M in LPS-stimulated RAW 264.7 cells was evaluated using LDH and MTT assays (Figure 2). None of the tested concentrations affected cell viability. Therefore, these concentrations were used in subsequent experiments.

3.2. Effect of 2B5H4M on LPS-Stimulated NO Production and iNOS and COX-2 Expression in RAW 264.7 Cells

The potential anti-inflammatory effects of 2B5H4M on NO production were investigated in LPS-stimulated RAW 264.7 cells. NO production was significantly higher in LPS-treated cells compared to controls (Figure 3). However, 2B5H4M treatment dose-dependently inhibited the effects of LPS. In particular, treatment with 150 μM 2B5H4M resulted in a 76.4% reduction in LPS-induced NO production in RAW 264.7 cells (Figure 3A).
RT-PCR (Figure 3B) and Western blotting (Figure 3C) were conducted to determine whether the inhibitory effect of 2B5H4M on NO production was associated with the regulation of iNOS and COX-2 expression. 2B5H4M markedly inhibited the LPS-induced upregulation of iNOS and COX-2 at both the mRNA and protein levels in a concentration-dependent manner, indicating that 2B5H4M suppresses NO production by downregulating these inflammatory enzymes and may thus act as an inhibitor of macrophage activation.

3.3. Effect of 2B5H4M on Cytokine Expression in RAW 264.7 Cells

LPS-stimulated RAW 264.7 cells were treated with 2B5H4M, and the expression of IL-6, IL-1β, and TNF-α was evaluated (Figure 4). 2B5H4M reduced the mRNA levels of these cytokines in a concentration-dependent manner, and similar inhibitory patterns were observed for LPS-induced cytokine production in the culture supernatants. These results indicate that 2B5H4M suppresses both the expression and secretion of major pro-inflammatory cytokines in activated macrophages.

3.4. Effect of 2B5H4M on MAPK Phosphorylation in RAW 264.7 Cells

To investigate the mechanism by which 2B5H4M inhibits the expression of pro-inflammatory mediators and cytokines, the effect of 2B5H4M on the MAPK signaling pathway was examined (Figure 5). In LPS-stimulated RAW 264.7 cells, 2B5H4M markedly suppressed LPS-induced phosphorylation of JNK and ERK, whereas the phosphorylation of p38 was not significantly affected.

3.5. Effect of 2B5H4M on NF-kB Activation in RAW 264.7 Cells

One of the most extensively studied signaling pathways associated with the inflammatory process is the NF-kB pathway. Therefore, the effect of 2B5H4M on the phosphorylation of NF-κB in LPS-stimulated RAW 264.7 cells was investigated. 2B5H4M inhibited the LPS-induced phosphorylation and degradation of IκB-α in a concentration-dependent manner (Figure 6A). Additionally, after only 30 min of stimulation, LPS induced the translocation of p65 and p50 from the cytoplasm to the nucleus of RAW 264.7 cells. Conversely, 2B5H4M treatment significantly inhibited the nuclear translocation of p65 and p50 (Figure 6B). These results suggested that 2B5H4M inhibits NF-kB activation by blocking the LPS-induced phosphorylation and degradation of IκB-α.
Taken together, these results indicate that 2B5H4M suppresses LPS-induced inflammatory responses in RAW 264.7 macrophages by inhibiting the production of pro-inflammatory mediators and cytokines through coordinated suppression of MAPK and NF-κB signaling pathways [32,33,34,35,36,37,38,39,40]. Marine-derived bromophenols, such as bis(2,3-dibromo-4,5-dihydroxybenzyl) ether (BDDE), have been reported to exert potent anti-inflammatory activity in macrophages by modulating NF-κB and MAPK signaling cascades [41,42]. Although 2B5H4M is not a naturally occurring marine metabolite, its brominated phenolic scaffold closely resembles those of algal bromophenols, suggesting that it may function as a synthetic, marine-inspired analogue. Consistent with this, 2B5H4M inhibited LPS-induced phosphorylation of ERK and JNK, suggesting that its anti-inflammatory effects are mediated through modulation of multiple intracellular signaling pathways.
In parallel, vanillin and related phenolic aldehydes have been reported to attenuate LPS- or infection-induced inflammation in vitro and in vivo by suppressing TLR4/NF-κB signaling and reducing pro-inflammatory cytokine production [28]. However, most of these investigations have focused either on natural marine phenolics or on non-brominated vanillin scaffolds, and brominated aldehydes structurally related to 2B5H4M remain poorly characterized in macrophage-based inflammation models. The present findings extend this body of work by demonstrating that 2B5H4M, a brominated vanillin derivative with a marine-inspired phenolic scaffold, concomitantly inhibits ERK/JNK phosphorylation and NF-κB activation in LPS-stimulated RAW 264.7 cells, thereby positioning 2B5H4M as a mechanistically relevant synthetic analogue within the broader context of marine phenolic and vanillin-derived anti-inflammatory agents.
This study has limitations, as the anti-inflammatory effects of 2B5H4M were evaluated only in vitro, and its in vivo efficacy and molecular targets remain to be elucidated. Future studies including in vivo validation and computational approaches such as molecular docking and molecular dynamics simulations may further clarify its pharmacological potential [21,23]. Such approaches would further support the potential of 2B5H4M as a marine-inspired anti-inflammatory lead compound.
In conclusion, 2B5H4M effectively inhibited LPS-induced inflammatory responses in RAW 264.7 macrophages by suppressing iNOS- and COX-2–mediated NO and PGE2 production, as well as pro-inflammatory cytokine expression, through inhibition of ERK/JNK and NF-κB signaling pathways.

Author Contributions

Conceptualization, J.K.; Formal analysis, E.-A.K.; Methodology, S.-Y.H.; Supervision, S.-J.H.; Visualization, N.K.; Writing—original draft, J.K.; Writing—review and editing, J.K. All authors have read and agreed to the published version of the manuscript.

Funding

This research was supported by research grants from the Korea Institute of Ocean Science and Technology (PEA0311, PEA0315).

Data Availability Statement

The original contributions presented in this study are included in the article. Further inquiries can be directed to the corresponding author.

Acknowledgments

The authors would like to thank the reviewers for their valuable comments and suggestions.

Conflicts of Interest

The authors declare no conflicts of interest.

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Phycology 06 00010 g001
Figure 1. Chemical structure of 2-Bromo-5-hydroxy-4-methoxybenzaldehyde (2B5HMB).
Figure 1. Chemical structure of 2-Bromo-5-hydroxy-4-methoxybenzaldehyde (2B5HMB).
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Figure 2. Effects of 2B5H4M on the viability and cytotoxicity of RAW 264.7 macrophages. Cells were treated with 2B5H4M (37.5, 75, and 150 μM) in the presence of LPS (1 μg/mL) for 24 h. Cell viability was measured using the MTT assay, and cytotoxicity was quantified by LDH release. Values are presented as mean ± SD (n = 3). Statistical differences were analyzed by one-way ANOVA followed by Dunnett’s post hoc test.
Figure 2. Effects of 2B5H4M on the viability and cytotoxicity of RAW 264.7 macrophages. Cells were treated with 2B5H4M (37.5, 75, and 150 μM) in the presence of LPS (1 μg/mL) for 24 h. Cell viability was measured using the MTT assay, and cytotoxicity was quantified by LDH release. Values are presented as mean ± SD (n = 3). Statistical differences were analyzed by one-way ANOVA followed by Dunnett’s post hoc test.
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Figure 3. Effect of 2B5H4M on LPS-induced nitric oxide (NO) production and inflammatory mediator expression in RAW 264.7 macrophages. (A) Nitrite levels in culture supernatants were measured by the Griess reaction as an indicator of NO production after cells were treated with LPS (1 μg/mL) and various concentrations of 2B5H4M for 24 h. (B) Protein expression levels of iNOS and COX-2 were analyzed by western blotting. (C) Densitometric analysis of iNOS and COX-2 protein expression normalized to the corresponding loading control. Data are expressed as mean ± SD (n = 3). Statistical comparisons were performed using one-way ANOVA followed by Dunnett’s post hoc test (* p < 0.05, ** p < 0.01 vs. LPS-treated group).
Figure 3. Effect of 2B5H4M on LPS-induced nitric oxide (NO) production and inflammatory mediator expression in RAW 264.7 macrophages. (A) Nitrite levels in culture supernatants were measured by the Griess reaction as an indicator of NO production after cells were treated with LPS (1 μg/mL) and various concentrations of 2B5H4M for 24 h. (B) Protein expression levels of iNOS and COX-2 were analyzed by western blotting. (C) Densitometric analysis of iNOS and COX-2 protein expression normalized to the corresponding loading control. Data are expressed as mean ± SD (n = 3). Statistical comparisons were performed using one-way ANOVA followed by Dunnett’s post hoc test (* p < 0.05, ** p < 0.01 vs. LPS-treated group).
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Figure 4. Effects of 2B5H4M on LPS-induced cytokine production (TNF-α, IL-1β, IL-6) in RAW 264.7 macrophages. Cytokine levels in supernatants were measured using ELISA kits after 24 h treatment. ** Values are mean ± SD (n = 3). Statistical differences were assessed using one-way ANOVA followed by Dunnett’s post hoc test (* p < 0.05, ** p < 0.01 vs. LPS-treated group).
Figure 4. Effects of 2B5H4M on LPS-induced cytokine production (TNF-α, IL-1β, IL-6) in RAW 264.7 macrophages. Cytokine levels in supernatants were measured using ELISA kits after 24 h treatment. ** Values are mean ± SD (n = 3). Statistical differences were assessed using one-way ANOVA followed by Dunnett’s post hoc test (* p < 0.05, ** p < 0.01 vs. LPS-treated group).
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Figure 5. Inhibition of LPS-induced MAPK phosphorylation by 2B5H4M in RAW 264.7 cells. Phosphorylated and total ERK and JNK levels were detected by western blotting. Data represent mean ± SD (n = 3). Statistical analysis was conducted using one-way ANOVA followed by Dunnett’s post hoc test (* p < 0.05 vs. LPS-treated group).
Figure 5. Inhibition of LPS-induced MAPK phosphorylation by 2B5H4M in RAW 264.7 cells. Phosphorylated and total ERK and JNK levels were detected by western blotting. Data represent mean ± SD (n = 3). Statistical analysis was conducted using one-way ANOVA followed by Dunnett’s post hoc test (* p < 0.05 vs. LPS-treated group).
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Figure 6. Effects of 2B5H4M on NF-κB signaling pathway activation in RAW 264.7 macrophages. (A) Degradation of IκB-α in cytosolic fractions following LPS stimulation and 2B5H4M treatment was analyzed by Western blotting. (B) Nuclear translocation of NF-κB p65/p50 was examined in nuclear extracts by Western blot analysis. Data are expressed as mean ± SD (n = 3). Statistical significance was determined using one-way ANOVA followed by Dunnett’s post hoc test (* p < 0.05, ** p < 0.01 vs. LPS-treated group).
Figure 6. Effects of 2B5H4M on NF-κB signaling pathway activation in RAW 264.7 macrophages. (A) Degradation of IκB-α in cytosolic fractions following LPS stimulation and 2B5H4M treatment was analyzed by Western blotting. (B) Nuclear translocation of NF-κB p65/p50 was examined in nuclear extracts by Western blot analysis. Data are expressed as mean ± SD (n = 3). Statistical significance was determined using one-way ANOVA followed by Dunnett’s post hoc test (* p < 0.05, ** p < 0.01 vs. LPS-treated group).
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MDPI and ACS Style

Kim, J.; Heo, S.-Y.; Kim, E.-A.; Kang, N.; Heo, S.-J. 2-Bromo-5-Hydroxy-4-Methoxybenzaldehyde Exhibits Anti-Inflammatory Effects Through the Inactivation of ERK, JNK, and NF-kB Pathways in RAW 264.7 Cells. Phycology 2026, 6, 10. https://doi.org/10.3390/phycology6010010

AMA Style

Kim J, Heo S-Y, Kim E-A, Kang N, Heo S-J. 2-Bromo-5-Hydroxy-4-Methoxybenzaldehyde Exhibits Anti-Inflammatory Effects Through the Inactivation of ERK, JNK, and NF-kB Pathways in RAW 264.7 Cells. Phycology. 2026; 6(1):10. https://doi.org/10.3390/phycology6010010

Chicago/Turabian Style

Kim, Junseong, Seong-Yeong Heo, Eun-A Kim, Nalae Kang, and Soo-Jin Heo. 2026. "2-Bromo-5-Hydroxy-4-Methoxybenzaldehyde Exhibits Anti-Inflammatory Effects Through the Inactivation of ERK, JNK, and NF-kB Pathways in RAW 264.7 Cells" Phycology 6, no. 1: 10. https://doi.org/10.3390/phycology6010010

APA Style

Kim, J., Heo, S.-Y., Kim, E.-A., Kang, N., & Heo, S.-J. (2026). 2-Bromo-5-Hydroxy-4-Methoxybenzaldehyde Exhibits Anti-Inflammatory Effects Through the Inactivation of ERK, JNK, and NF-kB Pathways in RAW 264.7 Cells. Phycology, 6(1), 10. https://doi.org/10.3390/phycology6010010

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