scholarly journals Chlorogenic Acid Potentiates the Anti-Inflammatory Activity of Curcumin in LPS-Stimulated THP-1 Cells

Nutrients ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2706 ◽  
Author(s):  
Akshay Bisht ◽  
Martin Dickens ◽  
Kay Rutherfurd-Markwick ◽  
Rohith Thota ◽  
Anthony N. Mutukumira ◽  
...  
Keyword(s):  
Cell Viability ◽  
Chlorogenic Acid ◽  
Mrna Expression ◽  
Inflammatory Marker ◽  
Pcr Analysis ◽  
Marker Genes ◽  
Dependent Manner ◽  
Major Barrier ◽  
Tnf Α ◽  
Anti Inflammatory

The anti-inflammatory effects of curcumin are well documented. However, the bioavailability of curcumin is a major barrier to its biological efficacy. Low-dose combination of complimentary bioactives appears to be an attractive strategy for limiting barriers to efficacy of bioactive compounds. In this study, the anti-inflammatory potential of curcumin in combination with chlorogenic acid (CGA), was investigated using human THP-1 macrophages stimulated with lipopolysaccharide (LPS). Curcumin alone suppressed TNF-α production in a dose-dependent manner with a decrease in cell viability at higher doses. Although treatment with CGA alone had no effect on TNF-α production, it however enhanced cell viability and co-administration with curcumin at a 1:1 ratio caused a synergistic reduction in TNF-α production with no impact on cell viability. Furthermore, an qRT-PCR analysis of NF-κB pathway components and inflammatory biomarkers indicated that CGA alone was not effective in reducing the mRNA expression of any of the tested inflammatory marker genes, except TLR-4. However, co-administration of CGA with curcumin, potentiated the anti-inflammatory effects of curcumin. Curcumin and CGA together reduced the mRNA expression of pro-inflammatory cytokines [TNF-α (~88%) and IL-6 (~99%)], and COX-2 (~92%), possibly by suppression of NF-κB (~78%), IκB-β-kinase (~60%) and TLR-4 receptor (~72%) at the mRNA level. Overall, co-administration with CGA improved the inflammation-lowering effects of curcumin in THP-1 cells.

scholarly journals Increased Anti-Inflammatory Effects on LPS-Induced Microglia Cells by Spirulina maxima Extract from Ultrasonic Process

2019 ◽  
Vol 9 (10) ◽  
pp. 2144 ◽  
Author(s):  
Woon Yong Choi ◽  
Jae-Hun Sim ◽  
Jung-Youl Lee ◽  
Do Hyung Kang ◽  
Hyeon Yong Lee
Keyword(s):  
Mrna Expression ◽  
Dependent Manner ◽  
Spirulina Maxima ◽  
Concentration Dependent Manner ◽  
Quantitative Correlation ◽  
Tnf Α ◽  
Ultrasonic Process ◽  
Anti Inflammatory ◽  
Low Cytotoxicity ◽  
High Concentrations

The Spirulina maxima exact from a non-thermal ultrasonic process (UE) contains 17.5 mg/g of total chlorophyll, compared to 6.24 mg/g of chlorophyll derived from the conventional 70% ethanol extraction at 80 °C for 12 h (EE). The UE also showed relatively low cytotoxicity against murine microglial cells (BV-2) and inhibited the production of the inflammatory mediators, NO and PGE2. The UE also effectively suppresses both mRNA expression and the production of pro-inflammatory cytokines, such as TNF-α, IL-6 and IL-1β, in a concentration-dependent manner. Notably, TNF-α gene and protein production were most strongly down-regulated, while IL-6 was the least affected by all ranges of treatment concentrations. This work first demonstrated a quantitative correlation between mRNA expression and the production of cytokines, showing that suppression of TNF-α gene expression was most significantly correlated with its secretion. These results clearly proved that the anti-inflammatory effects of Spirulina extract from a nonthermal ultrasonic process, which yielded high concentrations of intact forms of chlorophylls, were increased two-fold compared to those of conventional extracts processed at high temperature.

scholarly journals Alprostadil attenuates LPS-induced cardiomyocyte injury by inhibiting the Wnt5a/JNK/NF-κB pathway

Herz ◽  
2019 ◽  
Vol 45 (S1) ◽  
pp. 130-138 ◽  
Author(s):  
T. Yu ◽  
D. Dong ◽  
J. Guan ◽  
J. Sun ◽  
M. Guo ◽  
...  
Keyword(s):  
Cell Viability ◽  
Mrna Expression ◽  
Molecular Mechanisms ◽  
Quantitative Polymerase Chain Reaction ◽  
Cellular Damage ◽  
H9c2 Cells ◽  
Tnf Α ◽  
H9c2 Cardiomyocytes ◽  
Anti Inflammatory ◽  
Factor Α

Abstract Background Clinical research has demonstrated that alprostadil has an anti-inflammatory effect; however, to date, its molecular mechanisms remain unclear. This study aimed to examine the anti-inflammatory activity and related mechanisms of alprostadil in lipopolysaccharide (LPS)-treated H9c2 cells. Methods Cell morphology was observed under an inverted light microscope, while cell viability was assessed with the 3‑(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide (MTT) assay. Enzyme-linked immunosorbent assays (ELISA) were conducted to study biochemical indicators of cellular damage, such as released lactate dehydrase (LDH) and troponin, and inflammatory cytokine levels including interleukin-1β (IL-1β), IL-6, IL-17, and tumor necrosis factor-α (TNF-α). The mRNA expression levels of Wnt5a, c‑jun N‑terminal kinase (JNK), and nuclear factor kappa B (NF-κB) were further investigated by real-time quantitative polymerase chain reaction (RT-PCR). The effects of alprostadil on the Wnt5a/JNK/NF-κB pathway in H9c2 cells was examined by Western blotting. Results Alprostadil increased the cell viability of LPS-stimulated H9c2 cells, reduced LDH and troponin production, and attenuated IL-1β, IL-6, IL-17, and TNF-α secretion. Moreover, alprostadil reduced the mRNA expression of Wnt5a, JNK, and NF-κB and decreased the expression of Wnt5a, NF-κB, and the ratio of p‑JNK/JNK in H9c2 cells treated with LPS. The siWnt5a or JNK inhibitor SP600125 significantly augmented the inhibitory effects of alprostadil on the Wnt5a/JNK/NF-κB pathway. Conclusion Our results show that alprostadil has anti-inflammatory effects and could attenuate LPS-induced injury in H9c2 cardiomyocytes via the Wnt5a/JNK/NF-κB pathway.

scholarly journals Baicalin and Geniposide Inhibit Polarization and Inflammatory Injury of OGD/R-Treated Microglia by Suppressing the 5-LOX/LTB4 Pathway

2021 ◽  
Author(s):  
HuiMin Li ◽  
Yan Wang ◽  
Bin Wang ◽  
Min Li ◽  
JiPing Liu ◽  
...  
Keyword(s):  
Cell Viability ◽  
Lentiviral Vector ◽  
Glucose Deprivation ◽  
Binding Activity ◽  
Pcr Analysis ◽  
Dependent Manner ◽  
Western Blots ◽  
Inflammatory Injury ◽  
Ischemic Cerebrovascular Disease ◽  
Tnf Α

AbstractCerebral ischemia causes severe neurological disorders and neuronal dysfunction. Baicalin (BC), geniposide (GP), and their combination (BC/GP) have been shown to inhibit post-ischemic inflammatory injury by inhibiting the 5-LOX/CysLTs pathway. The aims of this study were to observe the inhibitory effects of BC/GP on the activation of microglial cells induced by oxygen glucose deprivation and reoxygenation (OGD/R) and to investigate whether the 5-LOX/LTB4 pathway was involved in these effects. Molecular docking showed that BC and GP exhibited considerable binding activity with LTB4 synthase LTA4H. BV-2 microglia were transfected with a 5-LOX overexpression lentiviral vector, and then OGD/R was performed. The effects of different concentrations of BC, GP, and BC/GP (6.25 μM, 12.5 μM, and 25 μM) on cell viability and apoptosis of microglia were evaluated by MTT and flow cytometry. The expression of TNF-α, IL-1β, NF-κB, and pNF-κB also was measured by ELISA, Western blots and immunofluorescence. Western blots and qRT-PCR analysis were used to determine the levels of CD11b, CD206, and 5-LOX pathway proteins. Results showed that BC, GP, and BC/GP reduced the apoptosis caused by OGD/R in a dose-dependent manner, and cell viability was significantly increased at a concentration of 12.5 μM. OGD/R significantly increased the release of TNF-α, IL-1β, NF-κB, pNF-κB, and CD11b. These effects were suppressed by BC, GP, and BC/GP, and the OGD/R-induced transfer of NF-κB p65 from the ctytoplasm to the nucleus was inhibited in microglia. Interestingly, the LTB4 inhibitor, U75302, exhibited the same effect. Also, BC, GP, and BC/GP significantly reduced the expression of 5-LOX pathway proteins. These results demonstrated that BC/GP inhibited OGD/R-induced polarization in BV2 microglia by regulating the 5-LOX/LTB4 signaling pathways and attenuating the inflammatory response. Our results supported the theoretical basis for additional in-depth study of the function of BC/GP and the value of determining its unique target, which might provide a new therapeutic strategy for ischemic cerebrovascular disease.

ANTI-INFLAMMATORY EFFECT OF PLANTAGO SP ETHANOLIC EXTRACT IN MURINE RAW264.7 MACROPHAGE CELLS

2018 ◽  
Vol 21 (02) ◽  
pp. 35-42 ◽  
Author(s):  
N V Ay ◽  
Altantsetseg Kh ◽  
Enkhchimeg V ◽  
Baatartsogt O
Keyword(s):  
Cell Viability ◽  
Mrna Expression ◽  
American Indians ◽  
Mrna Level ◽  
Inflammatory Activity ◽  
Pcr Analysis ◽  
No Production ◽  
Griess Reagent ◽  
Macrophage Cells ◽  
Anti Inflammatory

Besides being recorded as a traditional medicine, nowadays, plantain plants (Plantago sp.) are appreciated in many more aspects. Plantain is a name applied both to a drug and to a vegetable in a number of countries as Vietnam, China, Cambodia, Laos and North American Indians [9, 13]. Plantago sp. traditionally used for treating wound, fever and inflammation in Asia. This study aimed to investigate the anti-inflammatory activity of ethanolic extracts of Plantago sp. including P. major L. and P. depressa Willd. on RAW 264.7 murine macrophage cells. Cells were treated with different concentration of the PAE extract (50, 100, 200, 400 μg/mL) with or without lipopolysaccharide (LPS) stimulation to evaluate its effect on cell viability, using CCK-8 assay. Nitric oxide (NO) production was assessed by Griess reagent on LPS-stimulated cells using preceding PEE treatment. Furthermore, mRNA expression of inflammmatory-related genes were evaluated by RT-PCR analysis. The results revealed that PEE treatment increased cell viability in naive cells whereas inhibited cell profileration in LPS-stimulated cell dose-dependently. In addition, NO emission and mRNA level of IL-1β, IL-6, iNOS, COX-2 and NF-κB decreased by dose dependant manner. As summary, PEE exhibits anti-inflammatory activity through inhibition of pro-inflammatory mediators mRNA expression in macrophages.

scholarly journals TURMERIC EXTRACT POTENTIAL INHIBIT INFLAMMATORY MARKER IN LPS-STIMULATED MARCOPHAGE CELLS

2021 ◽  
pp. 7-11
Author(s):  
WAHYU WIDOWATI ◽  
DIANA KRISANTI JASAPUTRA ◽  
KAMILA YASHFA GUNAWAN ◽  
HANNA SARI WIDYA KUSUMA ◽  
SEILA ARUMWARDANA ◽  
...  
Keyword(s):  
Cell Line ◽  
Inflammatory Cytokines ◽  
Inflammatory Marker ◽  
Dependent Manner ◽  
Macrophage Cell Line ◽  
Macrophage Cell ◽  
Turmeric Extract ◽  
Tnf Α ◽  
Cox 2 ◽  
Anti Inflammatory

Objective: Inflammation can be induced by microbiological, chemical, physical factors and plays roles in inflammatory diseases. Turmeric (Curcuma longa L.) has been widely used to provide a diverse array of biological activities, including anti-inflammatory, antimicrobial, also antioxidant. The Turmeric extract (TE) anti-inflammatory potential was conducted using a Lipopolysaccharide (LPS)-induced RAW264.7 macrophage cell line by inhibiting inflammatory mediators especially IL-6, PGE-2, IL-1β, COX-2, TNF-α, iNOS, also NO level. Methods: The TE safe concentration in LPS-induced macrophage cell line was measured using MTS assay for further assay. The inflammatory markers (IL-6, PGE-2, COX-2, IL-1β, TNF-α, iNOS, NO) were measured using ELISA assay and NO by the nitrate/nitrite colorimetric assay in LPS-induced RAW264.7 cell line. LPS induced inflammatory marker by increasing inflammatory marker (IL-6, PGE-2, COX-2, IL-1β, TNF-α, iNOS, NO). Results: TE with 100 to 25 µg/ml, caused a significant reduction of cells viability, reaching only 30.27 % live cells. TE with lower concentrations (7.5; 5; 2.5 µg/ml) had no cytotoxic effect on macrophage cells (viability 117.31-131.08 %). LPS induction caused an increase in inflammatory cytokines IL-1β, PGE-2, IL-6, COX-2, TNF-α as well as iNOS and NO. Turmeric extract caused the reduction of the inflammatory cytokines in a dose-dependent manner. Conclusion: The research resulted that TE has anti-inflammatory activity by decreasing IL-6, PGE-2, COX-2, IL-1β, TNF-α, iNOS, and NO level on LPS-induced RAW264.7 cells.

Piper sarmentosum Roxb. Root Extracts Confer Neuroprotection by Attenuating Beta Amyloid-Induced Pro-Inflammatory Cytokines Released from Microglial Cells

2019 ◽  
Vol 16 (3) ◽  
pp. 251-260 ◽  
Author(s):  
Elaine Wan Ling Chan ◽  
Emilia Tze Ying Yeo ◽  
Kelly Wang Ling Wong ◽  
Mun Ling See ◽  
Ka Yan Wong ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Mrna Expression ◽  
Inflammatory Mediators ◽  
Beta Amyloid ◽  
Microglial Cells ◽  
Root Extracts ◽  
Tnf Α ◽  
P38α Mapk ◽  
Anti Inflammatory ◽  
Bv2 Microglial Cells

<P>Background: Alzheimer’s disease (AD) is a multifactorial neurodegenerative disorder that eventually leads to severe cognitive impairment. Although the exact etiologies of AD still remain elusive, increasing evidence suggests that neuroinflammation cascades mediated by microglial cells are associated with AD. Piper sarmentosum Roxb. (PS) is a medicinal plant reported to possess various biological properties, including anti-inflammatory, anti-psychotic and anti-oxidant activity. However, little is known about the anti-inflammatory activity of PS roots despite their traditional use to treat inflammatory- mediated ailments. Objective: This study aimed to evaluate the anti-inflammatory and neuroprotective properties of extracts obtained from the roots of PS against beta-amyloid (Aβ)-induced microglial toxicity associated with the production of pro-inflammatory mediators. Method: BV2 microglial cells were treated with hexane (RHXN), dichloromethane (RDCM), ethyl acetate (REA) and methanol (RMEOH) extracts of the roots of PS prior to activation by Aβ. The production and mRNA expression of pro-inflammatory mediators were evaluated by Griess reagent, ELISA kits and RT-qPCR respectively. The phosphorylation status of p38α MAPK was determined via western blot assay. BV2 conditioned medium was used to treat SH-SY5Y neuroblastoma cells and the neuroprotective effect was assessed using MTT assay. Results: PS root extracts, in particular RMEOH significantly attenuated the production and mRNA expression of IL-1β, IL-6 and TNF-α in Aβ-induced BV2 microglial cells. In addition, RHXN, REA and RMEOH extracts significantly reduced nitric oxide (NO) level and the inhibition of NO production was correlated with the total phenolic content of the extracts. Further mechanistic studies suggested that PS root extracts attenuated the production of cytokines by regulating the phosphorylation of p38α MAPK in microglia. Importantly, PS root extracts have protective effects against Aβ-induced indirect neurotoxicity either by inhibiting the production of NO, IL-1β, IL-6, and TNF-α in BV2 cells or by protecting SHSY5Y cells against these inflammatory mediators. Conclusions: These findings provided evidence that PS root extracts confer neuroprotection against Aβ- induced microglial toxicity associated with the production of pro-inflammatory mediators and may be a potential therapeutic agent for inflammation-related neurological conditions including Alzheimer’s disease (AD).</P>

scholarly journals Bioactivity-Guided Extract Optimization of Osmanthus fragrans var. aurantiacus Leaves and Anti-Inflammatory Activities of Phillyrin

Plants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1545
Author(s):  
Hwa-Young Song ◽  
Da-Eun Jeong ◽  
Mina Lee
Keyword(s):  
Biological Activities ◽  
Radical Scavenging ◽  
No Production ◽  
Dependent Manner ◽  
Optimal Method ◽  
Concentration Dependent Manner ◽  
Osmanthus Fragrans ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Extracellular Regulated Kinase

The aim of this study was to identify the optimal extraction conditions for leaves of Osmanthus fragrans var. aurantiacus. Inhibitory effects of various extracts on NO production were compared. Antioxidant evaluations for total phenol and flavonoid contents were carried out using various extracts of O. fragrans var. aurantiacus leaves obtained under optimal extraction conditions that showed the greatest effect on NO production. The optimal method for extracting O. fragrans var. aurantiacus leaves resulted in an extract named OP OFLE. OP OFLE showed DPPH and ABTS radical scavenging activities in a concentration-dependent manner. Phillyrin (PH) was isolated as a major compound from OP OFLE by HPLC/DAD analysis. OP OFLE and PH reduced inducible nitric oxide (iNOS) and cyclooxygenase (COX)-2 protein expression and downregulated proinflammatory cytokines such as interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor (TNF)-α in LPS-stimulated RAW 264.7 and HT-29 cells. To determine the signal pathway involved in the inhibition of NO production, a Western blot analysis was performed. Results showed that OP OFLE decreased phosphorylation of extracellular regulated kinase (pERK) 1/2 and the expression of nuclear factor-kappa B (NF-κB). Our results suggest that extracts of O. fragrans var. aurantiacus leaves and its major components have biological activities such as antioxidative and anti-inflammatory properties.

scholarly journals Targeting a Lipid Desaturation Enzyme, SCD1, Selectively Eliminates Colon Cancer Stem Cells through the Suppression of Wnt and NOTCH Signaling

Cells ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 106
Author(s):  
Yeongji Yu ◽  
Hyejin Kim ◽  
SeokGyeong Choi ◽  
JinSuh Yu ◽  
Joo Yeon Lee ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Notch Signaling ◽  
Cultured Cells ◽  
Pcr Analysis ◽  
Marker Genes ◽  
Dependent Manner ◽  
Lipid Desaturation ◽  
Novel Target

The elimination of the cancer stem cell (CSC) population may be required to achieve better outcomes of cancer therapy. We evaluated stearoyl-CoA desaturase 1 (SCD1) as a novel target for CSC-selective elimination in colon cancer. CSCs expressed more SCD1 than bulk cultured cells (BCCs), and blocking SCD1 expression or function revealed an essential role for SCD1 in the survival of CSCs, but not BCCs. The CSC potential selectively decreased after treatment with the SCD1 inhibitor in vitro and in vivo. The CSC-selective suppression was mediated through the induction of apoptosis. The mechanism leading to selective CSC death was investigated by performing a quantitative RT-PCR analysis of 14 CSC-specific signaling and marker genes after 24 and 48 h of treatment with two concentrations of an inhibitor. The decrease in the expression of Notch1 and AXIN2 preceded changes in the expression of all other genes, at 24 h of treatment in a dose-dependent manner, followed by the downregulation of most Wnt- and NOTCH-signaling genes. Collectively, we showed that not only Wnt but also NOTCH signaling is a primary target of suppression by SCD1 inhibition in CSCs, suggesting the possibility of targeting SCD1 against colon cancer in clinical settings.

scholarly journals Accumulation of Non-steroidal Anti-inflammatory Drugs by Gingival Fibroblasts

2006 ◽  
Vol 85 (5) ◽  
pp. 452-456 ◽  
Author(s):  
M.M. Zavarella ◽  
O. Gbemi ◽  
J.D. Walters
Keyword(s):  
Steady State ◽  
Connective Tissue ◽  
Inflammatory Mediator ◽  
Dependent Manner ◽  
Gingival Fibroblasts ◽  
Temperature Dependent ◽  
Tnf Α ◽  
Steady State Levels ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

Non-steroidal anti-inflammatory drugs (NSAIDs) are used to manage pain and inflammatory disorders. We hypothesized that gingival fibroblasts actively accumulate NSAIDs and enhance their levels in gingival connective tissue. Using fluorescence to monitor NSAID transport, we demonstrated that cultured gingival fibroblasts transport naproxen in a saturable, temperature-dependent manner with a Km of 127 μg/mL and a Vmax of 1.42 ng/min/μg protein. At steady state, the intracellular/extracellular concentration ratio was 1.9 for naproxen and 7.2 for ibuprofen. Naproxen transport was most efficient at neutral pH and was significantly enhanced upon cell treatment with TNF-α. In humans, systemically administered naproxen attained steady-state levels of 61.9 μg/mL in blood and 9.4 μg/g in healthy gingival connective tissue, while ibuprofen attained levels of 2.3 μg/mL and 1.5 μg/g, respectively. Thus, gingival fibroblasts possess transporters for NSAIDs that are up-regulated by an inflammatory mediator, but there is no evidence that they contribute to elevated NSAID levels in healthy gingiva.

Anti-inflammatory assessment of 3-Acetylmyricadiol in LPS-Stimulated Raw 264.7 Macrophages

2021 ◽  
Vol 24 ◽  
Author(s):  
Gazanfar Ahmad ◽  
Reyaz Hassan ◽  
Neerupma Dhiman ◽  
Asif Ali
Keyword(s):  
Nitric Oxide ◽  
Cell Viability ◽  
Ethyl Acetate ◽  
Mtt Assay ◽  
Bark Extract ◽  
Maximum Effect ◽  
Potential Candidate ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Inflammatory Action

Background: Pentacyclic triterpenoids are a biologically active class of phytoconstituents with diverse pharmacological activity including anti-inflammatory action. Objective: In the current study, we isolated 3-Acetylmyricadiol, a pentacyclic triterpenoid, from the ethyl acetate bark-extract of Myrica esculenta and evaluated it for anti-inflammatory potential. Methods: The ethyl acetate bark-extract of the M. esculenta was subjected to column chromatography to isolate 3-Acetylmyricadiol. MTT assay was performed to check cell viability. The production of proinflammatory mediators like Nitric oxide, IL-6, TNF-α was observed after administration of 5, 10, 20 μM of 3-Acetylmyricadiol in LPS-activated Raw 246.7 macrophages by the reported methods. Results: MTT assay indicated more than 90% cell viability up to 20 μM of 3-Acetylmyricadiol. The administration of 3-Acetylmyricadiol inhibited the production of Nitric oxide, IL-6, TNF-α in a dose-dependent manner significantly in comparison to LPS treated cells. The maximum effect was observed at 20 μM of 3-Acetylmyricadiol which resulted in 52.37, 63.10, 55.37 % inhibition of Nitric oxide, IL-6, TNF-α respectively. Conclusion: Our study demonstrated the anti-inflammatory action of 3-Acetylmyricadiol and can serve as a potential candidate in the development of the clinically efficient anti-inflammatory molecule.

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