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Molecular Mechanisms of Anti-inflammatory Natural Products

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Bioactives and Nutraceuticals".

Deadline for manuscript submissions: closed (30 December 2023) | Viewed by 6141

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Prof. Dr. Gi-Young Kim

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Guest Editor

Department of Marine Life Sciences, School of Marine Biomedical Sciences, Jeju National University, Jeju 63243, Republic of Korea
Interests: phytochemicals; nutraceuticals; antioxidant; cell death; inflammation; melanogenesis; bone formation
Special Issues, Collections and Topics in MDPI journals

Prof. Dr. Yung Hyun Choi

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Guest Editor

1. Department of Biochemistry, Dongeui University College of Korean Medicine, Busan 614‐052, Republic of Korea
2. Anti‐Aging Research Center, Dongeui University, Busan 614‐052, Republic of Korea
Interests: anti-inflammation; particulate matter; retinal inflammation; apoptosis; bioactive compounds

Special Issue Information

Dear Colleagues,

Inflammation is the body’s defense mechanism to external stimuli and is beneficial to the body. However, persistent inflammatory responses lead to chronic inflammation-related diseases such as atherosclerosis, rheumatoid arthritis, obesity, gout, Alzheimer’s disease, and cancer. Currently, steroidal and non-steroidal anti-inflammatory drugs (NSAIDs) have been commonly used to treat inflammatory diseases. However, these drugs can cause adverse effects, such as gastrointestinal damages, liver and kidney dysfunction, and skin diseases. Therefore, finding natural plant compounds without toxic side effects is a promising strategy to be solved in the clinical treatment of inflammation-related diseases. Hence, this topic will manage specific papers on the anti-oxidant and anti-inflammatory mechanisms of natural products at the molecular levels.

Prof. Dr. Gi-Young Kim
Prof. Dr. Yung Hyun Choi
Guest Editors

Manuscript Submission Information

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Keywords

anti-oxidant
anti-inflammation
reactive oxygen species
natural compounds
bioactive compounds

Published Papers (4 papers)

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Research

10 pages, 2621 KiB

Open AccessCommunication

Synergistic Effect of Saccharin and Caffeine on Antiproliferative Activity in Human Ovarian Carcinoma Ovcar-3 Cells

by Sun Ju Lee, Sang-Yong Park, Subin Bak, Min-Woo Lee, Dae Jin Lim, Hyeong-Dong Kim, Dong-Gil Kim and Suhng Wook Kim

Int. J. Mol. Sci. 2023, 24(19), 14445; https://doi.org/10.3390/ijms241914445 - 22 Sep 2023

Cited by 1 | Viewed by 1060

Abstract

The purpose of this study was to confirm the antiproliferative and apoptotic induction potential of a saccharin and caffeine combination in ovarian cancer cells. The cell line used was Ovcar-3, and the cell viability was measured through a WST-8 assay, while a Chou–Talalay assay was used to confirm the synergistic effect of saccharin and caffeine on the ovarian cancer cells. A clonogenic assay, annexin V-FITC/PI-PE double-staining, and RT-PCR were performed to confirm the expression of genes that induce colony formation, cell viability, and apoptosis in ovarian cancer cells treated with the saccharin–caffeine combination. It was demonstrated that both saccharin and caffeine decreased the viability of Ovcar-3 cells, and the cell viability decreased even more significantly when the cells were treated with the combination of saccharin and caffeine. The clonogenic assay results showed that the number of colonies decreased the most when saccharin and caffeine were combined, and the number of colonies also significantly decreased compared to the single-treatment groups. Based on flow cytometry analysis using annexin V-FITC/PI-PE double-staining, it was confirmed that the decrease in cell viability caused by the combination of saccharin and caffeine was correlated with the induction of apoptosis. The results of the RT-PCR confirmed that the combined treatment of saccharin and caffeine promoted cell apoptosis by regulating the expression of apoptosis-inducing genes. These results demonstrate that the combination of saccharin and caffeine more efficiently inhibits the proliferation of Ovcar-3 cells and induces apoptosis in vitro. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Anti-inflammatory Natural Products)

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17 pages, 3530 KiB

Open AccessArticle

Phytochemical Screening of Ultrasonic Extracts of Salix Species and Molecular Docking Study of Salix-Derived Bioactive Compounds Targeting Pro-Inflammatory Cytokines

by Emilia Gligorić, Ružica Igić, Branislava Teofilović and Nevena Grujić-Letić

Int. J. Mol. Sci. 2023, 24(14), 11848; https://doi.org/10.3390/ijms241411848 - 24 Jul 2023

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Abstract

Willow bark (Salix spp., Salicaceae) is a traditional analgesic and antirheumatic herbal medicine. The aim of this study was to evaluate and compare the phytochemical and antioxidant profiles of leaf and bark extracts of six species of the genus Salix obtained by ultrasound-assisted extraction (UAE) and to examine the inhibitory potential of target bioactive compounds against two inflammatory mediators, tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6), through in silico molecular docking. The total phenolic and flavonoid content of the extracts was estimated using spectrophotometric methods and the antioxidant activity using 2,2-diphenyl-1-picrylhydrazyl (DPPH^•) and hydroxyl radical (^•OH) scavenging assays. Chemical profiling of extracts was carried out using high-performance liquid chromatography coupled with a diode array detector (HPLC-DAD). Principal component analysis (PCA) was performed to differentiate the sample extracts based on their phytochemical profiles and amounts of target bioactive compounds. Chemical composition varied among the analyzed willow species and also among the plant organs of the same species. The major bioactive compounds of the extracts were salicin, chlorogenic acid, rutin and epicatechin. The extracts exhibited significant DPPH^● and ^●OH scavenging activities. Results of molecular docking revealed that chlorogenic acid had the highest binding affinity toward TNF-α and IL-6. UAE extracts represent valuable sources of antioxidant and anti-inflammatory compounds. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Anti-inflammatory Natural Products)

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12 pages, 3209 KiB

Open AccessArticle

Spermidine Attenuates High Glucose-Induced Oxidative Damage in Retinal Pigment Epithelial Cells by Inhibiting Production of ROS and NF-κB/NLRP3 Inflammasome Pathway

by EunJin Bang, Cheol Park, Hyun Hwangbo, Jung-Hyun Shim, Sun-Hee Leem, Jin Won Hyun, Gi-Young Kim and Yung Hyun Choi

Int. J. Mol. Sci. 2023, 24(13), 10550; https://doi.org/10.3390/ijms241310550 - 23 Jun 2023

Cited by 1 | Viewed by 1376

Abstract

Diabetic retinopathy (DR) is the leading cause of vision loss and a critical complication of diabetes with a very complex etiology. The build-up of reactive oxygen species (ROS) due to hyperglycemia is recognized as a primary risk factor for DR. Although spermidine, a naturally occurring polyamine, has been reported to have antioxidant effects, its effectiveness in DR has not yet been examined. Therefore, in this study, we investigated whether spermidine could inhibit high glucose (HG)-promoted oxidative stress in human retinal pigment epithelial (RPE) cells. The results demonstrated that spermidine notably attenuated cytotoxicity and apoptosis in HG-treated RPE ARPE-19 cells, which was related to the inhibition of mitochondrial ROS production. Under HG conditions, interleukin (IL)-1β and IL-18’s release levels were markedly increased, coupled with nuclear factor kappa B (NF-κB) signaling activation. However, spermidine counteracted the HG-induced effects. Moreover, the expression of nucleotide-binding oligomerization domain-like receptor (NLR) protein 3 (NLRP3) inflammasome multiprotein complex molecules, including TXNIP, NLRP3, ASC, and caspase-1, increased in hyperglycemic ARPE-19 cells, but spermidine reversed these molecular changes. Collectively, our findings demonstrate that spermidine can protect RPE cells from HG-caused injury by reducing ROS and NF-κB/NLRP3 inflammasome pathway activation, indicating that spermidine could be a potential therapeutic compound for DR treatment. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Anti-inflammatory Natural Products)

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16 pages, 4343 KiB

Open AccessArticle

Derrone Targeting the TGF Type 1 Receptor Kinase Improves Bleomycin-Mediated Pulmonary Fibrosis through Inhibition of Smad Signaling Pathway

by Ilandarage Menu Neelaka Molagoda, Sobarathne Senel Sanjaya, Kyoung Tae Lee, Yung Hyun Choi, Joyce H. Lee, Mi-Hwa Lee, Chang-Hee Kang, Chang-Min Lee and Gi-Young Kim

Int. J. Mol. Sci. 2023, 24(8), 7265; https://doi.org/10.3390/ijms24087265 - 14 Apr 2023

Cited by 2 | Viewed by 1689

Abstract

Transforming growth factor-β (TGF-β) has a strong impact on the pathogenesis of pulmonary fibrosis. Therefore, in this study, we investigated whether derrone promotes anti-fibrotic effects on TGF-β1-stimulated MRC-5 lung fibroblast cells and bleomycin-induced lung fibrosis. Long-term treatment with high concentrations of derrone increased the cytotoxicity of MRC-5 cells; however, substantial cell death was not observed at low concentrations of derrone (below 0.05 μg/mL) during a three-day treatment. In addition, derrone significantly decreased the expressions of TGF-β1, fibronectin, elastin, and collagen1α1, and these decreases were accompanied by downregulation of α-SMA expression in TGF-β1-stimulated MRC-5 cells. Severe fibrotic histopathological changes in infiltration, alveolar congestion, and alveolar wall thickness were observed in bleomycin-treated mice; however, derrone supplementation significantly reduced these histological deformations. In addition, intratracheal administration of bleomycin resulted in lung collagen accumulation and high expression of α-SMA and fibrotic genes—including TGF-β1, fibronectin, elastin, and collagen1α1—in the lungs. However, fibrotic severity in intranasal derrone-administrated mice was significantly less than that of bleomycin-administered mice. Molecular docking predicted that derrone potently fits into the ATP-binding pocket of the TGF-β receptor type 1 kinase domain with stronger binding scores than ATP. Additionally, derrone inhibited TGF-β1-induced phosphorylation and nuclear translocations of Smad2/3. Overall, derrone significantly attenuated TGF-β1-stimulated lung inflammation in vitro and bleomycin-induced lung fibrosis in a murine model, indicating that derrone may be a promising candidate for preventing pulmonary fibrosis. Full article

(This article belongs to the Special Issue Molecular Mechanisms of Anti-inflammatory Natural Products)

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