The effect of bitter gourd (Momordica charantia) ethanolic extract on inflammatory infiltrates and NF-κB activation in periodontitis

Periodontitis is a periodontal disease involving the gingiva, periodontal ligament, cementum, and alveolar bone due to an inflammatory process. Virulence factors of periodontopathogens and inflammatory responses in periodontitis can stimulate nuclear factor-kappa B (NF-κB) activity. Charantoside c and Momordicosides g in bitter gourd prevent NF-κB activation stimulated by TNF-α in HepG2 cells. This study aims to determine the effect of bitter gourd fruit (Momordica charantia) ethanolic extract as an anti-inflammatory substance on the level of inflammatory infiltrates and the number of cells that experience NF-κB activation in the periodontitis model. Eighty male Wistar rats were divided into 5 groups. The mandibular incisors were ligated for 14 days to induce periodontitis. Each group was given Momordica charantia extract of 500 mg/kg BW, 250 mg/kg BW, and 100 mg/kg BW; ibuprofen 100 mg/kg BW; and aquades orally using oral gavage on the day 14. Rat necropsy was carried out on day 1, 3, 5, and 7 after giving the substances. Taking out the lower jaw was done to make tissue preparations followed by staining them with hematoxylin eosin (HE). Immunohistochemicalanalysis was performed to observe cells that were positive for NF-κB activation. The results showed a decrease in the density of inflammatory infiltrates in all groups, except for those given aquades. The number of inflammatory cells ofneutrophils, macrophages, and lymphocytes that experienced NF-κB activation showed the most effective decrease in the group of Momordica charantia 500 mg/kg BW, on the 7th day. The conclusion of this study is that ethanolic extractof Momordica charantia has an anti-inflammatory effect and prevents the activation of NF-kB in rat gingival induced by periodontitis. The highest effect was found at a dose of 500 mg/kg BW on day 7 after giving of extracts.

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The Anti-Inflammatory Effects of Angiogenin in an Endotoxin Induced Uveitis in Rats

International Journal of Molecular Sciences ◽

10.3390/ijms21020413 ◽

2020 ◽

Vol 21 (2) ◽

pp. 413

Author(s):

Jihae Park ◽

Jee Taek Kim ◽

Soo Jin Lee ◽

Jae Chan Kim

Keyword(s):

Western Blot ◽

Inflammatory Cytokines ◽

Aqueous Humor ◽

Rat Model ◽

Inflammatory Responses ◽

Inflammatory Cells ◽

Ocular Tissue ◽

Tnf Α ◽

Anti Inflammatory

Angiogenin (ANG) is involved in the innate immune system and inflammatory disease. The aim of this study is to evaluate the anti-inflammatory effects of ANG in an endotoxin induced uveitis (EIU) rat model and the pathways involved. EIU rats were treated with balanced salt solution (BSS), a non-functional mutant ANG (mANG), or wild-type ANG (ANG). The integrity of the blood-aqueous barrier was evaluated by the infiltrating cell and protein concentrations in aqueous humor. Histopathology, Western blot, and real-time qRT-PCR of aqueous humor and ocular tissue were performed to analyze inflammatory cytokines and transcription factors. EIU treated with ANG had decreased inflammatory cells and protein concentrations in the anterior chamber. Compared to BSS and mANG, ANG treatment showed reduced expression of IL-1β, IL-8, TNF-α, and Myd88, while the expression of IL-4 and IL-10 was increased. Western blot of ANG treatment showed decreased expression of IL-6, inducible nitric oxide synthase (iNOS), IL-1β, TNF-α, and phosphorylated NF-κB and increased expression of IL-10. In conclusion, ANG seems to reduce effectively immune mediated inflammation in the EIU rat model by reducing the expression of proinflammatory cytokines, while increasing the expression of anti-inflammatory cytokines through pathways related to NF-κB. Therefore, ANG shows potential for effectively suppressing immune-inflammatory responses in vivo.

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A novel fluorinated stilbene exerts hepatoprotective properties in CCl4-induced acute liver damage

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y11-074 ◽

2011 ◽

Vol 89 (10) ◽

pp. 759-766 ◽

Cited By ~ 2

Author(s):

Horacio Rivera ◽

Martha S. Morales-Ríos ◽

Wendy Bautista ◽

Mineko Shibayama ◽

Víctor Tsutsumi ◽

...

Keyword(s):

Liver Damage ◽

Inflammatory Responses ◽

Acute Liver Damage ◽

Tnf Α ◽

Male Wistar Rats ◽

Anti Inflammatory ◽

Factor Α ◽

Glutamyl Transpeptidase

There has been a recently increase in the development of novel stilbene-based compounds with in vitro anti-inflamatory properties. For this study, we synthesized and evaluated the anti-inflammatory properties of 2 fluorinated stilbenes on carbon tetrachloride (CCl4)-induced acute liver damage. To achieve this, CCl4 (4 g·kg–1, per os) was administered to male Wistar rats, followed by either 2-fluoro-4′-methoxystilbene (FME) or 2,3-difluoro-4′-methoxystilbene (DFME) (10 mg·kg–1, per os). We found that although both of the latter compounds prevented cholestatic damage (γ-glutamyl transpeptidase activity), only DFME showed partial but consistent results in the prevention of necrosis, as assessed by both alanine aminotransferase activity and histological analysis. Since inflammatory responses are mediated by cytokines, mainly tumour necrosis factor α (TNF-α), we used the Western blot technique to determine the action of FME and DFME on the expression level of this cytokine. The observed increase in the level of TNF-α caused by CCl4 administration was only prevented by treatment with DFME, in agreement with our biochemical findings. This result was confirmed by measuring interleukin-6 (IL-6) levels, since the expression of this protein depends on the level of TNF-α. In this case, DFME completely blocked the CCl4-induced increase of IL-6. Our results suggest that DFME possesses greater anti-inflammatory properties in vivo than FME. DFME constitutes a possible therapeutic agent for liver disease and could serve as a template for structure optimization.

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Naringin and Hesperidin Counteract Diclofenac-Induced Hepatotoxicity in Male Wistar Rats via Their Antioxidant, Anti-Inflammatory, and Antiapoptotic Activities

Oxidative Medicine and Cellular Longevity ◽

10.1155/2021/9990091 ◽

2021 ◽

Vol 2021 ◽

pp. 1-14

Author(s):

Rasha A. Hassan ◽

Walaa G. Hozayen ◽

Haidy T. Abo Sree ◽

Hessah M. Al-Muzafar ◽

Kamal A. Amin ◽

...

Keyword(s):

Wistar Rats ◽

Liver Lipid ◽

Diclofenac Sodium ◽

Elevated Serum ◽

Inflammatory Cells ◽

Hepatic Necrosis ◽

Hydropic Degeneration ◽

Tnf Α ◽

Male Wistar Rats ◽

Anti Inflammatory

This study is aimed at evaluating the preventive effect and at suggesting the mode of actions of naringin and hesperidin and their combination in diclofenac-induced hepatotoxicity. Male Wistar rats, intraperitoneally injected with diclofenac sodium (3 mg/kg b.wt/day), were orally treated with naringin (20 mg/kg b.wt/day) and hesperidin (20 mg/kg b.wt/day) and their combination for 4 weeks. The administrations of naringin and hesperidin to diclofenac-injected rats led to a significant decrease in the elevated serum ALT, AST, LDH, ALP, GGT, total bilirubin, TNF-α, and IL-17 levels as well as liver lipid peroxidation and liver p53 and caspase-3 mRNA expressions. In contrast, serum IL-4 level, liver GSH content, and liver GPx and SOD activities increased. In association, diclofenac-induced deleterious histological alterations including hydropic degeneration, cytoplasmic vacuolization, apoptosis, and focal hepatic necrosis of hepatocytes associated with inflammatory cells’ infiltration were remarkably improved by treatments with naringin and hesperidin. In conclusion, naringin, hesperidin, and their combination, which was the most potent, counteract diclofenac-induced liver injury via antioxidant, anti-inflammatory, and antiapoptotic actions. Thus, this study recommends the use of naringin and hesperidin or their combination to resolve the side effects of drugs like diclofenac on the liver.

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Ethanolic extract of Achillea wilhelmsii C. Koch improves pulmonary function and inflammation in LPS-induced acute lung injury mice

Journal of Complementary and Integrative Medicine ◽

10.1515/jcim-2021-0045 ◽

2021 ◽

Vol 0 (0) ◽

Author(s):

Niloofar Honari ◽

Parastoo Shaban ◽

Saeed Nasseri ◽

Mehran Hosseini

Keyword(s):

Acute Lung Injury ◽

Lung Injury ◽

Inflammatory Cell ◽

Ethanolic Extract ◽

Inflammatory Cells ◽

Lavage Fluid ◽

Lps Challenge ◽

Tnf Α ◽

Anti Inflammatory ◽

Achillea Wilhelmsii

Abstract Objectives Acute lung injury (ALI) is a life-threatening pulmonary dysfunction associated with severe inflammation. There are still no effective pharmacological therapies for the treatment of ALI. In this concern, several anti-inflammatory agents could be used as add-on therapy to inhibit inflammation. Achillea wilhelmsii (AW) C. Koch is a well-known medicinal plant in the Iranian ethnomedical practices with anti-inflammatory activity. This study was aimed to evaluate the efficacy of ethanolic extract of AW on lipopolysaccharide (LPS)-induced ALI in mice. Methods The ALI model was established via the intra-tracheal (i.t.) administration of LPS (2 mg/kg) to male BALB/c mice. The ALI mice were divided into four groups (n=8 each) which intra-peritoneally (i.p.) treated with repeated doses of saline (model), dexamethasone (2 mg/kg), and AW (150–300 mg/kg) 1, 11 and 23 h post LPS administration. Twenty-four hours after the LPS challenge, bronchoalveolar lavage fluid (BALF) and lung tissue were evaluated for inflammatory cell influx, level of tumor necrosis factor-α (TNF-α) and histopathological changes. Results The AW (150–300 mg/kg) treated mice showed lower inflammatory cells infiltration in BALF and TNF-α level when compared to the model group. In addition, LPS induced several pathological alterations such as edema, alveolar hemorrhage and inflammatory cell infiltration into the interstitium and alveolar spaces. Treatment with AW significantly reduced LPS-induced pathological injury. Conclusions Taken together, the data here indicated that AW may be considered as a promising add-on therapy for ALI.

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Hyaluronic Acid-Modified and TPCA-1-Loaded Gold Nanocages Alleviate Inflammation

Pharmaceutics ◽

10.3390/pharmaceutics11030143 ◽

2019 ◽

Vol 11 (3) ◽

pp. 143 ◽

Cited By ~ 4

Author(s):

Jingnan Zhao

Keyword(s):

Hyaluronic Acid ◽

Inflammatory Cells ◽

Oxygen Species ◽

Necrosis Factor Alpha ◽

Tnf Α ◽

Nanogold Particles ◽

Gold Nanocages ◽

Factor Alpha ◽

Anti Inflammatory ◽

Necrosis Factor

Gold nanocages (AuNCs) are biocompatible and porous nanogold particles that have been widely used in biomedical fields. In this study, hyaluronic acid (HA) and peptide- modified gold nanocages (HA-AuNCs/T/P) loaded with 2-[(aminocarbonyl)amino]-5-(4-fluorophenyl)-3-thiophenecarboxamide (TPCA-1) were prepared to investigate their potential for combating inflammation. TPCA-1 was released from AuNCs, intracellularly when HA was hydrolyzed by hyaluronidase. HA-AuNCs/T/P show a much higher intracellular uptake than AuNCs/T/P, and exhibit a much higher efficacy on the suppression of tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) than free TPCA-1, suggesting great improvement to the anti-inflammatory efficacy of TPCA-1 through the application of AuNCs. HA-AuNCs/T/P can also reduce the production of reactive oxygen species in inflammatory cells. This study suggests that HA-AuNCs/T/P may be potential agents for anti-inflammatory treatment, and are worthy of further investigation.

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In Vitro Evaluation of the Anti-Inflammatory Effect of KMUP-1 and in Vivo Analysis of Its Therapeutic Potential in Osteoarthritis

Biomedicines ◽

10.3390/biomedicines9060615 ◽

2021 ◽

Vol 9 (6) ◽

pp. 615

Author(s):

Shang-En Huang ◽

Erna Sulistyowati ◽

Yu-Ying Chao ◽

Bin-Nan Wu ◽

Zen-Kong Dai ◽

...

Keyword(s):

Articular Cartilage ◽

Inflammatory Responses ◽

Therapeutic Potential ◽

Antioxidant Properties ◽

Serum Levels ◽

Gene Expressions ◽

Tnf Α ◽

Anti Inflammatory

Osteoarthritis is a degenerative arthropathy that is mainly characterized by dysregulation of inflammatory responses. KMUP-1, a derived chemical synthetic of xanthine, has been shown to have anti-inflammatory and antioxidant properties. Here, we aimed to investigate the in vitro anti-inflammatory and in vivo anti-osteoarthritis effects of KMUP-1. Protein and gene expressions of inflammation markers were determined by ELISA, Western blotting and microarray, respectively. RAW264.7 mouse macrophages were cultured and pretreated with KMUP-1 (1, 5, 10 μM). The productions of TNF-α, IL-6, MMP-2 and MMP- 9 were reduced by KMUP-1 pretreatment in LPS-induced inflammation of RAW264.7 cells. The expressions of iNOS, TNF-α, COX-2, MMP-2 and MMP-9 were also inhibited by KMUP-1 pretreatment. The gene expression levels of TNF and COX families were also downregulated. In addition, KMUP-1 suppressed the activations of ERK, JNK and p38 as well as phosphorylation of IκBα/NF-κB signaling pathways. Furthermore, SIRT1 inhibitor attenuated the inhibitory effect of KMUP-1 in LPS-induced NF-κB activation. In vivo study showed that KMUP-1 reduced mechanical hyperalgesia in monoiodoacetic acid (MIA)-induced rats OA. Additionally, KMUP-1 pretreatment reduced the serum levels of TNF-α and IL-6 in MIA-injected rats. Moreover, macroscopic and histological observation showed that KMUP-1 reduced articular cartilage erosion in rats. Our results demonstrated that KMUP-1 inhibited the inflammatory responses and restored SIRT1 in vitro, alleviated joint-related pain and cartilage destruction in vivo. Taken together, KMUP-1 has the potential to improve MIA-induced articular cartilage degradation by inhibiting the levels and expression of inflammatory mediators suggesting that KMUP-1 might be a potential therapeutic agent for OA.

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Evaluation of analgesic and anti-inflammatory activity of ethanolic extract of Enhydra fluctuans on male wistar rats

Journal of Applied Pharmaceutical Research ◽

10.18231/joapr.2021.9.1.37.42 ◽

2021 ◽

Vol 9 (1) ◽

pp. 1-7

Author(s):

Kishor Kumar Roy ◽

Md. Kabirul Islam Mollah ◽

Md. Masud Reja ◽

Dibyendu Shil ◽

Ranjan Kumar Maji

Keyword(s):

Wistar Rats ◽

Pain Threshold ◽

Ethanolic Extract ◽

Inflammatory Activity ◽

Paw Edema ◽

Hot Plate ◽

Plate Method ◽

Traditional System ◽

Male Wistar Rats ◽

Anti Inflammatory

Enhydra fluctuations an edible semi-aquatic vegetable plant are widely used in the traditional system of medicine. Ethanolic extract of Enhydra fluctuans was screened for analgesic & anti-inflammatory activity. Analgesic activity was evaluated by the hot plate method and anti-inflammatory activity was evaluated by formalin induce paw edema in Wistar rats (male). Ethanolic extract dose of 300 mg/kg reduce formalin induce paw inflammation and also increased the pain threshold in rats evidenced by hot plate method. The experimental results concluded that Enhydra fluctuans have significant analgesic and anti-inflammatory activity may due to flavonoid and phenolic compound content.

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Abstract 553: Siglec-1 (CD169) on Monocytes/Macrophages: A New Receptor For Extracellular Self-RNA in Triggering Inflammatory Responses via the Sheddase TACE/ADAM17

Arteriosclerosis Thrombosis and Vascular Biology ◽

10.1161/atvb.35.suppl_1.553 ◽

2015 ◽

Vol 35 (suppl_1) ◽

Author(s):

Hector A Cabrera-Fuentes ◽

Klaus T Preissner ◽

William A Boisvert

Keyword(s):

Inflammatory Cytokines ◽

Inflammatory Responses ◽

Transmembrane Protein ◽

Macrophage Polarization ◽

Extracellular Rna ◽

Tnf Α ◽

M1 Phenotype ◽

Phenotype Markers ◽

Anti Inflammatory

As an important component of atherosclerosis, monocytes/macrophages respond to external stimuli with rapid changes in their expression of many inflammation-related genes to undergo polarization towards the M1 (pro-inflammatory) or M2 (anti-inflammatory) phenotype. Although sialoadhesin (Sn), also known as SIGLEC-1 or CD169, is a transmembrane protein receptor expressed on monocytes and macrophages whether it has a role in macrophage polarization and ultimately, macrophage-driven atherogenesis, has not been investigated. We have previously shown that, independently of Toll-like receptor signaling, extracellular RNA (eRNA) could exert pro-thrombotic and pro-inflammatory properties in the cardiovascular system by inducing cytokine mobilization. In the current study, recombinant mouse macrophage CSF[[Unable to Display Character: –]]driven bone marrow-derived macrophage (BMDM) differentiation was found to be skewed towards the M1 phenotype by exposure of cells to eRNA. This resulted in up-regulation of inflammatory markers, whereas anti-inflammatory genes were significantly down-regulated by eRNA. Interestingly, eRNA was released from BMDM under hypoxia and induced TNF-α liberation by activating TNF-α converting enzyme (TACE) to provoke inflammation. Conversely, TNF-α promoted eRNA release, especially under hypoxia, feeding a vicious cycle of cell damage. Administration of RNase1 or TAPI (a TACE-inhibitor) prevented the production of inflammatory mediators. Murine BMDM isolated from mice deficient in sialoadhesin had the opposite reaction to eRNA treatment with a prominent down-regulation of pro-inflammatory cytokines/M1 phenotype markers, while anti-inflammatory cytokines/M2 phenotype markers were significantly raised. In keeping with the proposed role of eRNA as a pro-inflammatory “alarm signal”, these data further shed light on the role of eRNA in macrophage function in the context of chronic inflammatory diseases such as atherosclerosis. The identification of sialoadhesin as putative eRNA recognition site on macrophages may allow further investigation of the underlying mechanisms of eRNA-macrophage interaction and related signal transduction pathways. Siglec-1 thereby may provides a new target to treat eRNA-mediated vascular diseases.

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Phytosterols Suppress Phagocytosis and Inhibit Inflammatory Mediators via ERK Pathway on LPS-Triggered Inflammatory Responses in RAW264.7 Macrophages and the Correlation with Their Structure

Foods ◽

10.3390/foods8110582 ◽

2019 ◽

Vol 8 (11) ◽

pp. 582 ◽

Cited By ~ 5

Author(s):

Yuan ◽

Zhang ◽

Shen ◽

Jia ◽

Xie

Keyword(s):

Nitric Oxide ◽

Inflammatory Responses ◽

Ester Group ◽

No Production ◽

Raw264.7 Macrophages ◽

Extracellular Signal ◽

Tnf Α ◽

Anti Inflammatory ◽

Factor Α ◽

Oxide Synthase

Phytosterols, found in many commonly consumed foods, exhibit a broad range of physiological activities including anti-inflammatory effects. In this study, the anti-inflammatory effects of ergosterol, β-sitosterol, stigmasterol, campesterol, and ergosterol acetate were investigated in lipopolysaccharide (LPS)-induced RAW264.7 macrophages. Results showed that all phytosterol compounds alleviated the inflammatory reaction in LPS-induced macrophage models; cell phagocytosis, nitric oxide (NO) production, release of tumor necrosis factor-α (TNF-α), and expression and activity of pro-inflammatory mediator cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and phosphorylated extracellular signal-regulated protein kinase (p-ERK) were all inhibited. The anti-inflammatory activity of β-sitosterol was higher than stigmasterol and campesterol, which suggests that phytosterols without a double bond on C-22 and with ethyl on C-24 were more effective. However, inconsistent results were observed upon comparison of ergosterol and ergosterol acetate (hydroxy or ester group on C-3), which suggest that additional research is still needed to ascertain the contribution of structure to their anti-inflammatory effects.

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