Anti-inflammatory activity of Camellia japonica oil

Kim, Seung Beom; Jung, Eun Sun; Shin, Seung Woo; Kim, Moo Han; Kim, Young Soo; Lee, Jong; Park, Deok Hoon

doi:10.5483/bmbrep.2012.45.3.177

Cited by 33 publications

(27 citation statements)

References 34 publications

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“…20,55 Monokine induced by INF-c expression is significantly decreased after topical application of anti-inflammatory substances, such as 5-aminoimidazole-4-carboxamide-1-b-d-ribofuranoside and adiponectin. 34,46 We suspect that inhibition of the NF-jB signaling pathway by the CJ extracts, as proven by Kim S et al 2 led to the decreased expression of anti-inflammatory cytokines and chemokines observed in this work.…”

Section: Discussionmentioning

confidence: 62%

“…2 The anti-inflammatory action of CJ extracts also was shown in this study. Western blot analysis performed during the in vitro study demonstrated that CJ extracts exert antiinflammatory effects by decreasing the expression of COX-2 The expression of COX-2 is upregulated in the ocular surface after injury and during inflammation.…”

Section: Discussionmentioning

confidence: 71%

“…Subsequently, the cells were pretreated with either different concentrations of CJ extracts (0.001%, 0.01%, and 0.1% diluted in PBS) for 1 hour or PBS only as a negative control, followed by rinsing, and then reincubation for another 24 hours. Water-soluble tetrazolium salt reagent solution (10 lL) then was added to each well, and the plate was reincubated for 3 hours in a CO 2 incubator. An ELx808 absorbance microplate reader (BioTek, Winooski, VT, USA) was used to measure the absorbance at 570 nm.…”

Section: Culture Of Hce Cells and Cell Viability Assaymentioning

confidence: 99%

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Anti-Inflammatory and Antioxidative Effects of Camellia japonica on Human Corneal Epithelial Cells and Experimental Dry Eye: In Vivo and In Vitro Study

Lee

Choi

Cui

et al. 2017

Invest. Ophthalmol. Vis. Sci.

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Citation: Lee HS, Choi J-H, Cui L, et al. Anti-inflammatory and antioxidative effects of Camellia japonica on human corneal epithelial cells and experimental dry eye: in vivo and in vitro study. Invest Ophthalmol Vis Sci. 2017;58:119658: -120758: . DOI:10.1167 PURPOSE. To analyze the anti-inflammatory and antioxidative effects of Camellia japonica (CJ) on human corneal epithelial (HCE) cells and its therapeutic effects in a mouse model of experimental dry eye (EDE). METHODS.Camellia japonica extracts of varying concentrations (0.001%, 0.01%, and 0.1%) were used to treat HCE cells. Dichlorofluorescein diacetate (DCF-DA) and dihydroethidium (DHE) assays were performed. The production of peroxiredoxin (PRX) 1-6 and manganesedependent superoxide dismutase (MnSOD) in HCE cells was assessed using Western blot analysis. Furthermore, eye drops containing 0.001%, 0.01%, or 0.1% CJ extract or a balanced salt solution (BSS) were applied to the EDE. Clinical parameters were measured 7 days after treatment. The levels of inflammatory markers and intracellular reactive oxygen species (ROS) were measured.RESULTS. Treatment with 0.01% and 0.1% CJ extracts decreased apoptosis in HCE cells. In addition, band intensities of PRX 1, 4, and 5, as well as MnSOD, after hydrogen peroxide (H 2 O 2 ) treatment showed a significant improvement after pretreatment with 0.01% and 0.1% CJ extracts. Mice treated with 0.1% CJ extract showed significantly improved clinical parameters when compared to those of the EDE control and BSS groups. A significant decrease in the levels of inflammatory markers and intracellular ROS was observed in the 0.01% and 0.1% CJ extract groups.CONCLUSIONS. Camellia japonica extracts promoted antioxidative protein expression and suppressed apoptosis in HCE cells. Furthermore, CJ extracts improved clinical signs of dry eye and reduced oxidative stress and the expression of inflammatory markers, suggesting that eye drops containing CJ extract could be used as an adjunctive treatment for dry eye.

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Section: Discussionmentioning

confidence: 62%

Section: Discussionmentioning

confidence: 71%

Section: Culture Of Hce Cells and Cell Viability Assaymentioning

confidence: 99%

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Anti-Inflammatory and Antioxidative Effects of Camellia japonica on Human Corneal Epithelial Cells and Experimental Dry Eye: In Vivo and In Vitro Study

Lee

Choi

Cui

et al. 2017

Invest. Ophthalmol. Vis. Sci.

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“…Since nitric oxide (NO) is one of the inflammatory mediators, inflammation is characterized by the secretion of NO, and modulation of NO is considered a possible treatment for inflammatory disease (3). The increase in inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 causes cell damage following the increased production of NO and prostaglandins (PGs) (4). Suppressing the induction of COX-2 is a new strategy in the prevention of inflammation and COX-2 expression is also related to the activities of many intracellular signaling proteins, such as extracellular signal-regulated kinase (ERK), mitogen-activated protein kinase (MAPK), and Jun-N terminal kinase (JNK) (5).…”

Section: Introductionmentioning

confidence: 99%

Binding model for eriodictyol to Jun-N terminal kinase and its anti-inflammatory signaling pathway

Lee¹,

Jeong²,

Shin³

et al. 2013

BMB Reports

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The anti-inflammatory activity of eriodictyol and its mode of action were investigated. Eriodictyol suppressed tumor necrosis factor (mTNF)-α, inducible nitric oxide synthase (miNOS), interleukin (mIL)-6, macrophage inflammatory protein (mMIP)-1, and mMIP-2 cytokine release in LPS-stimulated macrophages. We found that the anti-inflammatory cascade of eriodictyol is mediated through the Toll-like Receptor (TLR)4/CD14, p38 mitogen-activated protein kinases (MAPK), extracellular-signalregulated kinase (ERK), Jun-N terminal kinase (JNK), and cyclooxygenase (COX)-2 pathway. Fluorescence quenching and saturation-transfer difference (STD) NMR experiments showed that eriodictyol exhibits good binding affinity to JNK, 8.79 × 105 M-1. Based on a docking study, we propose a model of eriodictyol and JNK binding, in which eriodictyol forms 3 hydrogen bonds with the side chains of Lys55, Met111, and Asp169 in JNK, and in which the hydroxyl groups of the B ring play key roles in binding interactions with JNK. Therefore, eriodictyol may be a potent anti-inflammatory inhibitor of JNK. [BMB Reports 2013; 46(12): 594-599]

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“…NO is generated through nitric oxide synthases enzyme (iNOS), while PGE 2 is produced by cyclooxygenase-2 enzyme (COX-2) (9). The expression of iNOS and COX-2 are regulated via mitogen activated protein kinase (MAPK) signaling pathways (10-12).…”

Section: Introductionmentioning

confidence: 99%

Floridoside suppresses pro-inflammatory responses by blocking MAPK signaling in activated microglia

Kim¹,

Li²,

Dewapriya³

et al. 2013

BMB Reports

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Inflammatory conditions mediated by activated microglia lead to chronic neuro-degenerative diseases such as Alzheimer’s, Parkinson’s, and Huntington’s diseases. This study was conducted to determine the effect of floridoside isolated from marine red algae Laurencia undulata on LPS (100 ng/ml) activated inflammatory responses in BV-2 microglia cells. The results show that floridoside has the ability to suppress pro-inflammatory responses in microglia by markedly inhibiting the production of nitric oxide (NO) and reactive oxygen species (ROS). Moreover, floridoside down-regulated the protein and gene expression levels of iNOS and COX-2 by significantly blocking the phosphorylation of p38 and ERK in BV-2 cells. Collectively, these results indicate that floridoside has the potential to be developed as an active agent for the treatment of neuro-inflammation. [BMB Reports 2013; 46(8): 398-403]

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Anti-inflammatory activity of Camellia japonica oil

Cited by 33 publications

References 34 publications

Anti-Inflammatory and Antioxidative Effects of Camellia japonica on Human Corneal Epithelial Cells and Experimental Dry Eye: In Vivo and In Vitro Study

Anti-Inflammatory and Antioxidative Effects of Camellia japonica on Human Corneal Epithelial Cells and Experimental Dry Eye: In Vivo and In Vitro Study

Binding model for eriodictyol to Jun-N terminal kinase and its anti-inflammatory signaling pathway

Floridoside suppresses pro-inflammatory responses by blocking MAPK signaling in activated microglia

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