Gastroprotective activity of Loranthus acaciae flower extract in a rodent model of ethanol-induced ulcer

Loranthus acaciae (Loranthaceae) is a perennial green semi-parasitic plant used in ethnopharmacological medicine for healing wounds. The protective effect of L. acaciae on gastric ulcer induced by ethanol was investigated in a rat model. Ulcer index and total glutathione level were measured and histological and immunohistochemical studies for the expression of cyclooxygenase-2 were performed. Furthermore, chemical constituents of the flower extract were analyzed. Ulcer index was significantly lowered in L. acaciae-treated groups. Protection ratios were 75.9%, 98.9%, and 70.7% for 250 mg/kg and 500 mg/kg of L. acaciae and 40 mg/kg of esomeprazole, respectively. Histological examination revealed fewer hemorrhage in mucosa and less edema in submucosa of L. acaciae-treated groups compared with control. In the esomeprazole-treated group, there was mild disruption in the surface epithelium and mild hemorrhage. However, edema and leucocytes infiltration in the submucosa layer were present. Immunohistochemical staining of stomach sections for cyclooxygenase-2 (COX-2) was negative in the control group as well as in the L. acaciae-treated groups. Total glutathione level in mucosa layer of the stomach was higher in L. acaciae-treated groups compared with control. Liquid chromatography-mass spectrometric analysis revealed the presence of loranthin and rutin as the major constituents. It can be concluded that L. acaciae imparted a gastroprotective action against ethanol-induced ulcer in rats. Novelty 500 mg/kg L. acaciae protected the stomach by 98.9% from ulcerogenic effect of ethanol. L. acaciae increased total glutathione level but not COX-2 expression in gastric mucosa. Loranthin and rutin were the major constituents in L. acaciae flower extract.

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Release of Cyclooxygenase-2 and Lipoxin A4 from Blood Leukocytes in Aspirin-exacerbated Respiratory Disease

Allergy & Rhinology ◽

10.2500/ar.2016.7.0172 ◽

2016 ◽

Vol 7 (3) ◽

pp. ar.2016.7.0172

Author(s):

Ajnacska Rozsasi ◽

Akos Heinemann ◽

Tilman Keck

Keyword(s):

Respiratory Disease ◽

Mononuclear Cells ◽

Cyclooxygenase 2 ◽

Control Group ◽

Peripheral Blood Mononuclear ◽

Control Subjects ◽

Aspirin Exacerbated Respiratory Disease ◽

Blood Mononuclear Cells ◽

Cox 2 ◽

The Difference

Background The release of cyclooxygenase-2 (COX-2) and lipoxin A4 (LXA4) from blood mononuclear cells in patients with aspirin-exacerbated respiratory disease (AERD) is only partially understood. Objective To investigate the presence of COX-2 and LXA4 in peripheral blood mononuclear cells (PBMC) derived from patients with AERD and with nasal polyps (NP) (designated as the AERD-NP group), patients with NP without AERD (the NP group), and healthy controls without sinus disease (the control group). Methods Blood was taken from 14 patients in the AERD-NP group, 6 patients in the NP group, and 8 healthy subjects in the control group. After culturing of human PBMC, the presence of COX-2 protein and LXA4 (ELISA) was detected in the supernatant, and the results were compared among the groups. Results COX-2 and LXA4 were detectable after culturing of PBMC in all patients in the AERD-NP and NP groups and in the control subjects. COX-2 was highest in the patients in the AERD-NP group, but the difference was not significant compared with patients with non-AERD polyp and with the control subjects. LXA4 was also highest in the AERD-NP group, but the difference was also not significant compared with the patients who were non-AERD polyp and the control subjects. Conclusion Neither the release of COX-2 or LXA4 was different between the patients with AERD and with NPs, the patients without AERD and with NPs, and the healthy control group. The release of these proteins in AERD needs further investigation.

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Association of a genetic variant (rs689466) of Cyclooxygenase-2 gene with chronic periodontitis in a sample of Iraqi population

Journal of Baghdad College of Dentistry ◽

10.26477/jbcd.v31i4.2719 ◽

2019 ◽

Vol 31 (4) ◽

Author(s):

Suha A. Dahash ◽

Maha Sh. Mahmood

Keyword(s):

Chronic Periodontitis ◽

Venous Blood ◽

Chronic Inflammatory Disease ◽

Cyclooxygenase 2 ◽

Control Group ◽

Case Group ◽

Pocket Depth ◽

Probing Pocket Depth ◽

Cox 2 ◽

Age Range

Background: periodontitis is a chronic inflammatory disease causing destruction of the tooth supporting structures, initiated by dental plaque and modified by environmental and genetic risk factors. Cyclooxygenase-2 (COX-2) enzyme is responsible for the production of prostaglandin E2, an important mediator in the chronic periodontitis (CP) pathogenesis. Polymorphisms in COX-2 gene have linked to CP in different populations. Aim: To study the association between Cyclooxygenase-2 single nucleotide polymorphism rs689466 (-1195A/G SNP) and chronic periodontitis in a sample of Iraqi population. Methods: One hundred Iraqi subjects divided into two groups: case group consisted of 70 CP patient (35 males and 35 females) with age range 30-55 years, and control group consisted of 30 racially matched healthy subjects (15 males and 15 females) with age range 30-50 years. Clinical periodontal parameters including plaque index (PLI), gingival index (GI), bleeding on probing (BOP), probing pocket depth (PPD) and clinical attachment level (CAL) were recoded for all participants. 3ml of venous blood was collected from each participant for isolating genomic DNA. Genotyping of the rs689466 in COX-2 gene was performed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. Results: The frequency of G allele carriers was significantly more prevalent in the case group compared to control group (P= 0.041), and allele G was associated with greater susceptibility for chronic periodontitis compared to allele A (OR=1.4). Conclusion: COX-2 (rs689466) polymorphism may be associated with increased chronic periodontitis susceptibility.

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Protective Effect of Quercetin, a Flavonol against Benzo(a)pyrene-Induced Lung Injury via Inflammation, Oxidative Stress, Angiogenesis and Cyclooxygenase-2 Signalling Molecule

Applied Sciences ◽

10.3390/app11188675 ◽

2021 ◽

Vol 11 (18) ◽

pp. 8675

Author(s):

Mohammad A. Alzohairy ◽

Amjad Ali Khan ◽

Mohammad Azam Ansari ◽

Ali Yousif Babiker ◽

Mohammed A. Alsahli ◽

...

Keyword(s):

Oxidative Stress ◽

Antioxidant Enzymes ◽

Treatment Group ◽

Lung Injury ◽

Inflammatory Cytokines ◽

Cyclooxygenase 2 ◽

Inflammatory Factors ◽

Control Group ◽

Cox 2

Quercetin (Qu) is an important polyphenolic flavonoid which exhibits tremendous antioxidant, anti-inflammatory and other health promoting effects. The aim of the current study was to explore the therapeutic role of Qu on benzo(a)pyrene [B(a)P]-induced lung injury in rats. B(a)P was given to the rats at dose of 50 mg/kg b.w. for continues 8 weeks through oral gavage. The rats were treated with Qu at dose of 50 mg/kg b.w prior 30 min before the oral administration of B(a)P. The effects of Qu were studied by measuring the level of lactate dehydrogenase (LDH), anti-oxidant enzymes, lipid peroxidation, inflammatory cytokines, lung tissues architecture and expression of cyclooxygenase-2 (COX-2). The level of pro‑inflammatory cytokines such as IL-1β (27.30 vs. 22.80 pg/mL), IL-6 (90.64 vs. 55.49 pg/mL) and TNF-α (56.64 vs. 40.49 pg/mL) increased significantly and antioxidant enzymes decreased significantly in benzopyrene-induced lung injury in comparison to the control group. The treatment with Qu potentially reversed the effects of B(a)P to a great extent, as it led to the enhancement of antioxidant enzymes and decreased proinflammatory cytokines level. A significant surge of VEGF level was noticed in the B(a)P group as compared to the control group, while the Qu treatment groups exhibited less angiogenesis as lower level of VEGF levels, compared with the B(a)P treatment group. The Qu treatment significantly decreased the degrees of histopathological changes and collagen deposition in B(a)P-induced lung injury. The B(a)P-treated group showed higher cytoplasmic expression of COX-2 protein, which significantly decreased in the Qu treatment group. These outcomes recommend an effective role of Qu in the protection of lung injury against B(a)P through the regulation of the inflammatory factors, oxidative stress and the maintenance lung tissue architecture.

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Evaluation of Cyclooxygenase-2 and p53 Expression in Pterygium Tissue Following Preoperative Intralesional Ranibizumab Injection

Frontiers in Medicine ◽

10.3389/fmed.2021.733523 ◽

2021 ◽

Vol 8 ◽

Author(s):

Ahmad Razif Omar ◽

Mohtar Ibrahim ◽

Hasnan Jaafar ◽

Ab Hamid Siti-Azrin ◽

Embong Zunaina

Keyword(s):

Cyclooxygenase 2 ◽

Control Group ◽

Control Groups ◽

P53 Expression ◽

Anti Vegf ◽

Significant Difference ◽

Pterygium Surgery ◽

Pterygium Excision ◽

Cox 2 ◽

And Control

Introduction: Overexpression of vascular endothelial growth factor (VEGF), cyclooxygenase-2 (COX-2), and p53 are the postulated aetiopathogenesis in pterygium. VEGF is responsible for the induction of COX-2 expression, whereas p53 plays an important role in the regulation of VEGF. This study aimed to evaluate the immunohistochemistry of COX-2 and p53 expressions from excised pterygium tissue from patients who received intralesional ranibizumab (anti-VEGF) injection 2 weeks prior to pterygium surgery.Materials and Methods: An interventional comparative study involving patients presenting with primary pterygium was conducted between September 2015 and November 2017. The patients were randomized into either the intervention or control group. Patients in the intervention group were injected with intralesional ranibizumab (0.5 mg/0.05 ml) 2 weeks prior to surgery. Both groups underwent pterygium excision followed by conjunctival autograft. Immunohistochemistry staining was performed to evaluate COX-2 and p53 expressions in the excised pterygium tissue.Results: A total of 50 patients (25 in both the intervention and control groups) were recruited. There were 34 (68%) patients with grade III pterygium and 16 (32%) patients with grade IV pterygium. There was statistically significant difference in reduction of COX-2 expression in the epithelial layer [84.0% (95% CI: 63.9, 95.5)] (p = 0.007) and stromal layer [84.0% (95% CI: 63.9, 95.5)] (p < 0.001) between intervention and control groups. There was no significant difference in the reduction of p53 expression between the two groups.Conclusion: This study demonstrated the possible use of intralesional anti-VEGF treatment prior to pterygium excision as a potential future modality of adjunctive therapy for pterygium surgery.

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Role of nitric oxide and cyclooxygenase-2 in regulating the renal hemodynamic response to norepinephrine

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00449.2002 ◽

2003 ◽

Vol 284 (2) ◽

pp. R488-R493 ◽

Cited By ~ 16

Author(s):

Ruth López ◽

María T. Llinás ◽

Francisco Roig ◽

F. Javier Salazar

Keyword(s):

Nitric Oxide ◽

Cyclooxygenase 2 ◽

Control Group ◽

Hemodynamic Effects ◽

Synthesis Inhibitor ◽

Renal Vasculature ◽

Renal Vasoconstriction ◽

Renal Hemodynamic ◽

Anesthetized Dogs ◽

Cox 2

We have reported that the renal hemodynamic effects of norepinephrine (NE) are modulated by cyclooxygenase-2 (COX-2)-derived metabolites. Our main objective was to examine whether there is an interaction between nitric oxide (NO) and COX-2 in modulating the renal hemodynamic effects of NE. NE was infused at three doses to anesthetized dogs pretreated with vehicle ( n = 8), a selective COX-2 inhibitor (nimesulide) ( n = 6), an NO synthesis inhibitor [ N G-nitro-l-arginine methyl ester;l-NAME] ( n = 8), or with nimesulide andl-NAME ( n = 5). During NE infusion, PGE2 excretion increased (125%) in the control group and did not change in the l-NAME-treated dogs. The simultaneous inhibition of NO and COX-2 potentiated to a greater extent the NE-induced renal vasoconstriction than inhibition of either NO or COX-2. The NE-induced renal vasoconstriction during NO and COX-2 inhibition was reduced ( P < 0.05) by infusing an AT1 receptor antagonist ( n = 6). These results suggest that there is an interaction between NO and COX-2 in protecting the renal vasculature from the NE effects and that angiotensin II partly mediates the NE-induced renal vasoconstriction when NO synthesis and COX-2 activity are reduced.

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Cyclooxygenase 2 and Lipoxin A4 in Nasal Polyps in Cystic Fibrosis

American Journal of Rhinology and Allergy ◽

10.2500/ajra.2011.25.3726 ◽

2011 ◽

Vol 25 (6) ◽

pp. e251-e254 ◽

Cited By ~ 5

Author(s):

Ajnacska Rozsasi ◽

Akos Heinemann ◽

Tilman Keck

Keyword(s):

Cystic Fibrosis ◽

Nasal Polyps ◽

Nasal Polyposis ◽

Inferior Turbinate ◽

Cyclooxygenase 2 ◽

Sinus Surgery ◽

Control Group ◽

Epithelial Cultures ◽

Cox 2 ◽

Tissue Specimens

Background The etiology of nasal polyps (NPs) and sinusitis in cystic fibrosis (CF) patients is still unknown. This study investigates the presence of cyclooxygenase 2 (COX-2) and lipoxin A 4 ( LXA 4) in epithelial cultures derived from NPs and turbinates in patients with CF and without CF. Methods NPs and turbinates were evaluated from eight CF patients with obstructing NPs undergoing sinus surgery. NPs and tissue from the hypertrophic inferior turbinate from 14 patients without history of CF undergoing sinus surgery served as control specimens. After tissue culturing, the presence of COX-2 protein and LXA 4 ( ELISA) was detected in CF polyps and turbinates and compared with that of the control group. Results COX-2 and LXA 4 were detectable in tissue specimens of all CF patients and control patients. COX-2 was highest in CF polyps, but the difference was not significant compared with CF turbinates or polyps and turbinates of patients not suffering from CF. LXA 4, however, was significantly higher in CF NPs compared with CF turbinate tissue. Compared with NPs of patients not having CF disease, CF polyps showed markedly higher concentrations of LXA 4. Conclusion LXA 4 is significantly elevated in CF NPs, whereas COX-2 is only slightly increased. The present data support the concept that LXA 4 plays an important role in CF nasal polyposis. Chronic infection in nasal polyposis and, because of inflammation, induced COX-2 in CF NPs may be related to increased LXA 4. The suspected interaction of COX-2 and LXA 4 needs further investigation.

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Apoptotic with Double-Staining Test, P53, and Cyclooxygenase-2 to Proliferation Colon Cancer Cell (WiDr) of Dolichol in Three Mangrove Leaves

Open Access Macedonian Journal of Medical Sciences ◽

10.3889/oamjms.2020.3289 ◽

2020 ◽

Vol 8 (A) ◽

pp. 37-42

Author(s):

Meighina Atika Istiqomah ◽

Mohammad Basyuni ◽

Poppy Anjelisa Zaitun Hasibuan

Keyword(s):

Cancer Cell ◽

Chemical Constituents ◽

Positive Control ◽

Cyclooxygenase 2 ◽

Double Staining ◽

M1 Phase ◽

Cancer Cell Growth ◽

Nypa Fruticans ◽

Genes Expression ◽

Cox 2

BACKGROUND: Mangroves secondary metabolites are mostly consisting of sterols, ubiquinones, isoprenoids, and polyisoprenoids. Polyisoprenoid is divided into two types, namely, polyprenol and dolichol, which has been reported to have biological and pharmacological activities. AIM: This research was aimed to analyze apoptosis 48 h with double staining and immunocytochemistry (ICC) 48 h of P53 and cyclooxygenase-2 (COX-2) gene expression from chemical constituents of dolichol in three mangrove leaves of Ceriops tagal, Nypa fruticans, and Rhizophora mucronata. METHODS: Apoptosis with the double-staining method was employed to analyze the genes expression in growth and development of cancer cells, P53, and COX-2 with ICC and flow cytometry method. The data were statistically analyzed using one-way ANOVA parametric statistical analysis followed by Duncan’s test. RESULTS: The result revealed that the increased apoptosis of samples C. tagal was 70% fluorescence orange, while N. fruticans and R. mucronata were 35% and 30% fluorescence orange, respectively. However, it was compared with the positive control; it produced orange fluorescent as much as 75%, suggesting that C. tagal have a position similar to 5-FU. Predominance dolichol in N. fruticans and C. tagal leaves led the expression gene of p53 to have 1.57% M1 phase, indicating the domination in G0-G1 phase (70–80%). Inhibit the expression for 48 h in p53 and COX-2 showing that n-hexane extract of C. tagal had the most percentage (80.733 ± 0.11%) to upregulate the p53 and less percentage (20.16 ± 1.19%) to downregulate the COX-2, indicating positive extract belong to N. fruticans and R. mucronata leaves. CONCLUSION: The present study confirmed the pharmacological properties of dolichol from three mangrove leaves as an anticancer of tumor suppressor genes and significantly proliferated of cancer cell growth from mangrove leaves.

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Aflatoxin B1-Induced COX-2 Expression Promotes Mitophagy and Contributes to Lipid Accumulation in Hepatocytes In Vitro and In Vivo

International Journal of Toxicology ◽

10.1177/1091581820939081 ◽

2020 ◽

Vol 39 (6) ◽

pp. 594-604

Author(s):

Xin-Lu Ren ◽

Peiyu Han ◽

Yiteng Meng

Keyword(s):

Aflatoxin B1 ◽

Hepg2 Cells ◽

Cyclooxygenase 2 ◽

Control Group ◽

Hepatocyte Steatosis ◽

Mitochondrial Lipid ◽

Cox 2 ◽

Elevated Lipid

Aim: Aflatoxin B1 (AFB1) is hepatotoxic. Numerous studies have shown that mitochondria play an essential role in AFB1-induced steatosis. However, the mechanisms of AFB1-induced steatosis via mitochondria are still obscure. The present study aimed to confirm that AFB1 causes hepatocyte steatosis regulated by cyclooxygenase-2 (COX-2)-induced mitophagy, both in vivo and in vitro. Methods: Adult male C57BL/6 mice were randomly divided into control group with the same volume of peanut oil and exposure group administered 0.6 mg/kg AFB1 once in 2 days for 1 month. HepG2 and Cas9-PTGS2 cells were treated with 5 μM AFB1 for 48 hours. Then, various indicators were evaluated. Results: Aflatoxin B1 causes liver injury and steatosis with increased alanine aminotransferase, aspartate aminotransferase, total cholesterol, total triglyceride levels in vivo and in vitro, and elevated lipid droplets in HepG2 cells. Cyclooxygenase-2 and mitophagy pathway were induced by AFB1 in both liver tissues and cultured HepG2 cells. Further studies have shown that knockout of COX-2 with the CRISPR/Cas9 system inhibited the AFB1-induced mitophagy and steatosis in HepG2 cells. Also, the inhibition of PTEN-induced putative kinase with RNA interference attenuated the AFB1-induced steatosis. Conclusions: The results of the current study suggested that AFB1 increases the expression of COX-2, which, in turn, elevates the level of mitophagy, thereby disrupting the normal mitochondrial lipid metabolism and causing steatosis. Thus, this study implies that COX-2 may be a potential target for therapy against AFB1-induced steatosis.

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