Ameliorative Effects of Caffeic Acid Phenethyl Ester on an Eccentric Exercise-Induced Skeletal Muscle Injury by Down-Regulating NF-kB Mediated Inflammation

Shen, Yuh Chiang; Yen, Jiin Cherng; Liou, Kuo Tong

doi:10.1159/000348412

Cited by 21 publications

(40 citation statements)

References 34 publications

(45 reference statements)

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“…In the present study, whereas 8-OhDG was strongly expressed in MTX group, reduction in 8-OhDG expression in the group for which MTX was administered together with hesperidin suggested that DNA damage was diminished and, hence, hesperidin had a protective property. NfKB, however, is a molecule which is activated when oxidative stress is developed [45,46] . It was reported that level of NfKB increased with testicular intoxication [47,48] .…”

Section: Discussionmentioning

confidence: 99%

Ratlarda Metoraksat Kaynaklı Testiküler Toksisite Üzerine Hesperidinin Etkisi

Belhan¹,

Özkaraca²,

Kandemir³

et al. 2017

Kafkas Univ Vet Fak Derg

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Citation of This ArticleBelhan S, Özkaraca M, Kandemir FM, Gülyüz F, Yıldırım S, Ömür AD, Yener Z: Effectiveness of hesperidin on methotrexate-induced testicular toxicity in rats. Kafkas Univ Vet Fak Derg, 23 (5): 789-796, 2017789-796, . DOI: 10.9775/kvfd.2017 AbstractThe aim of this study was to investigate the effect of hesperidin on male reproductive system in rats to which methotrexate (MTX) was administered. In the study, 28 male Wistar albino rats at the age of 8 weeks and had 250-300 g of live weight were used. Four experimental groups were formed; Group 1 (n=7): The control group, only feed and water were given. Group 2 (n=7): MTX group, a single dose of 20 mg/ kg of i.p. MTX was administered. Group 3 (n=7): Hesperidin group, 200 mg/kg of hesperidin was administered by gavage for 7 days. Group 4: MTX + hesperidin group (n=7): Following administration of a single dose of 20 mg/kg i.p. MTX , 200 mg/kg of Hesperidin was administered by oral gavage for 7 days. At the end of the experiment, rats were decapitated and biochemical, histopathological and spermatological parameters were examined. It was observed that in the MTX group, sperm motility and density, the enzymes CAT, GPx and SOD and GSH level decreased, TNF-alpha and IL-1 Beta, as well as MDA, levels were increased, regular structure of spermatogenic cells was impaired, and seminiferous tubules became necrotic and degenerative. It was determined that spermatological parameters improved and, necrotic and degenerative changes diminished by the administration of MTX+hesperidin. These outcomes indicated that hesperidin had a protective effect on destructive effects of MTX in rat testiclesv. Keywords: Male rat, Hesperidin, Methotrexate, Sperm, Reproductive system Ratlarda Metoraksat Kaynaklı Testiküler Toksisite Üzerine Hesperidinin Etkisi ÖzetBu çalışmanın amacı, metoraksat (MTX) uygulanan ratlarda hesperidinin erkek üreme sistemi üzerindeki etkisini araştırmaktı. Çalışmada 8 haftalık yaşta, 250-300 g canlı ağırlığa sahip 28 erkek Wistar albino cinsi rat kullanıldı. Dört deney grubu oluşturuldu; Grup 1 (n=7): kontrol grubu, sadece yem ve su verildi. Grup 2 (n=7): MTX grubu, 20 mg/kg MTX i.p. tek doz uygulandı. Grup 3 (n=7): Hesperidin grubu, 200 mg/kg hesperidin 7 gün süre ile ağızdan sonda yardımıyla verildi. Grup 4 (n=7): MTX + hesperidin grubu, 20 mg/kg MTX i.p tek doz uygulamasını takiben 200 mg/kg hesperidin 7 gün süre ile ağızdan sonda yardımıyla verildi. Deney sonunda ratlar dekapite edilerek biyokimyasal, histopatolojik ve spermatolojik parametreler incelendi. MTX grubunda sperm motilitesi ve yoğunluğunun, CAT, GPx ve SOD enzimlerinin ve GSH düzeyinin düştüğü, TNF-alpha ve IL-1 Beta ile MDA düzeyinin arttığı, spermatojenik hücrelerin düzenli yapısının bozulduğu, seminifer tubullerin nekrotik ve dejeneratif bir hal aldığı gözlendi. MTX + hesperidin uygulaması ile spermatolojik parametrelerin düzeldiği, nekrotik ve dejeneratif değişikliklerin azaldığı tespit edildi. Bu sonuçlar hesperidinin rat testislerinde MTX tarafından oluşan yıkıcı etkiler üze...

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Section: Discussionmentioning

confidence: 99%

Ratlarda Metoraksat Kaynaklı Testiküler Toksisite Üzerine Hesperidinin Etkisi

Belhan¹,

Özkaraca²,

Kandemir³

et al. 2017

Kafkas Univ Vet Fak Derg

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“…CAPE, which blocked the NF-κB-dependent activation of the inflammatory response (34). In another in vitro study, CAPE significantly suppressed the levels of lipopolysaccharide (LPS)-induced IL-1β, TNF-α and MCP-1 from a macrophage cell line, RAW264.7 (35).…”

Section: Anti-inflammatory Effects Of Capementioning

confidence: 95%

“…As a consequence of this inhibition, the activity of COX-1 and -2 and the activation of the COX-2 gene expression are suppressed (32,33). Recently, the protective effect of CAPE on a model of eccentric exercise-induced muscle injury was investigated (34). The study results showed that inflammatory skeletal muscle injury enhanced the expression of COX-2 and iNOS, as well as the production of IL-1β and monocyte chemoattractant protein-1 (MCP-1).…”

Section: Anti-inflammatory Effects Of Capementioning

confidence: 99%

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Therapeutic potential of caffeic acid phenethyl ester and its anti-inflammatory and immunomodulatory effects (Review)

Armutçu

Akyol

Üstünsoy

et al. 2015

Experimental and Therapeutic Medicine

129

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Abstract. Caffeic acid phenethyl ester (CAPE), a naturally occurring compound isolated from propolis extract, has been reported to have a number of biological and pharmacological properties, exerting antioxidant, anti-inflammatory, anticarcinogenic, antibacterial and immunomodulatory effects. Recent in vivo and in vitro study findings have provided novel insights into the molecular mechanisms involved in the anti-inflammatory and immunomodulatory activities of this natural compound. CAPE has been reported to have anti-inflammatory properties involving the inhibition of certain enzyme activities, such as xanthine oxidase, cyclooxygenase and nuclear factor-κB (NF-κB) activation. Since inflammation and immune mechanisms play a crucial role in the onset of several inflammatory diseases, the inhibition of NF-κB represents a rationale for the development of novel and safe anti-inflammatory agents. The primary goal of the present review is to highlight the anti-inflammatory and immunomodulatory activities of CAPE, and critically evaluate its potential therapeutic effects. Contents1. Introduction 2. Overview to the inflammatory response 3. Proinflammatory cytokines and signaling pathways 4. Anti-inflammatory effects of CAPE 5. Immunomodulatory effects of CAPE 6. Conclusion IntroductionCaffeic acid phenethyl ester (CAPE) is an important active component of honeybee propolis extract and has been used in traditional medicine for a number of years. CAPE is a polyphenol that contains hydroxyl groups within a catechol ring, the molecular formula of CAPE is C 17 H 16 O 4 (1,2) (Fig. 1). It has been shown that this active component of propolis possesses anti-inflammatory, immunomodulatory, antineoplastic, antioxidant and wound-healing properties (1-4). Inflammation is induced by the release of chemical mediators from damaged tissue and migratory cells. Mediators identified in the inflammatory process include biogenic amines, metabolites of arachidonic acid (eicosanoids), platelet aggregation factors, cytokines [interleukins (ILs) and tumor necrosis factor-α (TNF-α)] and free oxygen radicals. These substances are produced by inflammatory cells, such as polymorphonuclear leukocytes (neutrophils, eosinophils and basophils), endothelial cells, mast cells, macrophages, monocytes and lymphocytes (5,6). CAPE inhibits cytokine and chemokine production, the proliferation of T cells and lymphokine production, and thus suppresses the inflammatory process. Specifically, CAPE is a potent and a specific inhibitor of nuclear factor-κB (NF-κB) activation, and this may provide the molecular basis for its multiple anti-inflammatory and immunomodulatory activities (2,7). The aim of this review is to highlight the anti-inflammatory and immunomodulatory activities of CAPE, focusing on the mechanisms of action (already identified) underlying this activity. Overview to the inflammatory responseInflammation is an immunological response to pathogens and damage that is initiated to protect the body, and contributes Abbreviations: CAPE, caffeic acid phen...

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“…EXERCISE INDUCES INFLAMMATORY and stress signaling in muscle, including NF-B and JNK activation (17,39). These pathways drive the expression of proinflammatory genes such as IL-6 and chemokines such as chemokine C-C motif ligand 2 (CCL2)/monocyte chemoattractant protein-1 (MCP-1), and chemokine C-X-C motif ligands 1 and 5 (CXCL1/5) (23,33,39,43,44).…”

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confidence: 99%

Contracting C₂C₁₂ myotubes release CCL2 in an NF-κB-dependent manner to induce monocyte chemoattraction

Miyatake

Bilan

Pillon

et al. 2016

American Journal of Physiology-Endocrinology and Metabolism

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Miyatake S, Bilan PJ, Pillon NJ, Klip A. Contracting C2C12 myotubes release CCL2 in an NF-B-dependent manner to induce monocyte chemoattraction. Am J Physiol Endocrinol Metab 310: E160 -E170, 2016. First published November 10, 2015; doi:10.1152/ajpendo.00325.2015.-Muscle inflammation following exercise is characterized by expression of inflammatory cytokines and chemokines. Exercise also increases muscle macrophages derived from circulating monocytes. However, it is unknown whether muscle cells themselves attract circulating monocytes, or what is the underlying mechanism. We used an in vitro system of electrical stimulation (ES) causing C 2C12 myotube contraction to explore whether monocyte chemoattraction ensues and investigated the mediating chemoattractants. Conditioned medium from ES-contracted myotubes caused robust chemoattraction of THP-1 monocytes across Boyden chambers. Following ES, expression of several known monocyte chemokines [C-C motif ligand 2 (CCL2) and C-X-C motif ligand (CXCL)1, -2, and -5] was elevated, but of these, only recombinant CCL2 effectively reproduced monocyte migration. Electrically stimulated myotubes secreted CCL2, and neutralization of CCL2 in conditioned medium or antagonizing the CCL2 receptor (CCR2) in THP-1 monocytes inhibited ES-induced monocyte migration. N-benzyl-p-toluene sulfonamide (BTS), a myosin II-ATPase inhibitor, prevented ES-induced myotube contraction but not CCL2 gene expression and secretion. The membrane-permeant calcium chelator BAPTA-AM reduced ESinduced CCL2 secretion. Hence, electrical depolarization, rather than mechanical contraction, drives the rise in CCL2, with partial calcium input. ES activated the NF-B pathway; NF-B inhibitors reduced ES-induced CCL2 gene expression and secretion and repressed ESinduced THP-1

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Ameliorative Effects of Caffeic Acid Phenethyl Ester on an Eccentric Exercise-Induced Skeletal Muscle Injury by Down-Regulating NF-kB Mediated Inflammation

Cited by 21 publications

References 34 publications

Ratlarda Metoraksat Kaynaklı Testiküler Toksisite Üzerine Hesperidinin Etkisi

Ratlarda Metoraksat Kaynaklı Testiküler Toksisite Üzerine Hesperidinin Etkisi

Therapeutic potential of caffeic acid phenethyl ester and its anti-inflammatory and immunomodulatory effects (Review)

Contracting C₂C₁₂ myotubes release CCL2 in an NF-κB-dependent manner to induce monocyte chemoattraction

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Ameliorative Effects of Caffeic Acid Phenethyl Ester on an Eccentric Exercise-Induced Skeletal Muscle Injury by Down-Regulating NF-kB Mediated Inflammation

Cited by 21 publications

References 34 publications

Ratlarda Metoraksat Kaynaklı Testiküler Toksisite Üzerine Hesperidinin Etkisi

Ratlarda Metoraksat Kaynaklı Testiküler Toksisite Üzerine Hesperidinin Etkisi

Therapeutic potential of caffeic acid phenethyl ester and its anti-inflammatory and immunomodulatory effects (Review)

Contracting C2C12 myotubes release CCL2 in an NF-κB-dependent manner to induce monocyte chemoattraction

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Contracting C₂C₁₂ myotubes release CCL2 in an NF-κB-dependent manner to induce monocyte chemoattraction