scholarly journals Protective effects of caffeic acid phenethyl ester on radiation induced lung injury in rats

2008 ◽  
Vol 31 (5) ◽  
pp. 242 ◽  
Author(s):  
Oguz Galip Yildiz ◽  
Serdar Soyuer ◽  
Recep Saraymen ◽  
Celalettin Eroglu
Keyword(s):  
Radiation Therapy ◽  
Lung Injury ◽  
Caffeic Acid ◽  
Radiation Treatment ◽  
Caffeic Acid Phenethyl Ester ◽  
Albino Rats ◽  
Protective Effects ◽  
Sod Activity ◽  
Radiation Induced

Purpose: The prevention of radiation-induced pulmonary toxicity may help to improve radiation therapy in the cancer patient. The aim of this study was to investigate the pulmonary protective effects of caffeic acid phenethyl ester (CAPE), an antioxidant, on radiation-induced lung injury in rats. Methods:30 Wistar albino rats were divided into three groups and treated with saline, Radiation (RT) and RT + CAPE respectively. All rats were treated with CAPE (50 ?mol/kg i.p.) or saline. The first dose of CAPE was injected 24 h before radiation and application continued daily, with radiation in second day and 2 days more after the radiation treatment. Radiation dose was 800 cGy for total body. At 72 hr after the last radiation application, under general anesthesia using ip ketamine, the lungs were removed immediately after decapitation. After sacrification, antioxidant enzymes catalase (CAT), superoxide dismutase (SOD) activities and malondiadehyde (MDA) levels were evaluated in lung tissue. Results: The level of malondialdehyde (MDA) was higher in the RT group (233.4±1.5 nmol/g protein) than in both the control (131.8±0.92) and the RT + CAPE (151.4±1.8) groups (P < 0.001). However, CAT activity was decreased in the RT group (7.26±0.27 Umg protein) compared with control (8.49±0.51) and increased again in the RT + CAPE group (8.31±0.56; P < 0.001). In accord with CAT activity, SOD activity in the RT group (0.42±0.07 nmolMDA/g wet tissue) was different from the control (0.78±0.02) and RT + CAPE (0.86±0.06) groups (P < 0.001). Conclusion: CAPE aplication with radiation therapy attenuated radiation induced pulmonary injury in vivo, possibly by its antioxidant effect.

scholarly journals Caffeic Acid Phenethyl Ester Protects against Amphotericin B Induced Nephrotoxicity in Rat Model

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Atila Altuntaş ◽  
H. Ramazan Yılmaz ◽  
Ayşegül Altuntaş ◽  
Efkan Uz ◽  
Murat Demir ◽  
...  
Keyword(s):  
Caffeic Acid ◽  
Amphotericin B ◽  
Left Kidney ◽  
Caffeic Acid Phenethyl Ester ◽  
Control Group ◽  
Albino Rats ◽  
Sod Activity ◽  
Rat Models ◽  
Propolis Extract ◽  
The Right

The present study was conducted to investigate whether caffeic acid phenethyl ester (CAPE), an active component of propolis extract, has a protective effect on amphotericin B induced nephrotoxicity in rat models. Male Wistar-Albino rats were randomly divided into four groups: (I) control group (n = 10), (II) CAPE group (n = 9) which received 10 μmol/kg CAPE intraperitoneally (i.p.), (III) amphotericin B group (n = 7) which received one dose of 50 mg/kg amphotericin B, and (IV) amphotericin B plus CAPE group (n = 7) which received 10 μmol/kg CAPE i.p. and one dose of 50 mg/kg amphotericin B. The left kidney was evaluated histopathologically for nephrotoxicity. Levels of malondialdehyde (MDA), nitric oxide (NO), enzyme activities including catalase (CAT), and superoxide dismutase (SOD) were measured in the right kidney. Histopathological damage was prominent in the amphotericin B group compared to controls, and the severity of damage was lowered by CAPE administration. The activity of SOD, MDA, and NO levels increased and catalase activity decreased in the amphotericin B group compared to the control group (P=0.0001,P=0.003,P=0.0001, andP=0.0001, resp.). Amphotericin B plus CAPE treatment caused a significant decrease in MDA, NO levels, and SOD activity (P=0.04,P=0.02, andP=0.0001, resp.) and caused an increase in CAT activity compared with amphotericin B treatment alone (P=0.005). CAPE treatment seems to be an effective adjuvant agent for the prevention of amphotericin B nephrotoxicity in rat models.

scholarly journals Protective Effects of Intralipid and Caffeic Acid Phenethyl Ester on Nephrotoxicity Caused by Dichlorvos in Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Muhammet Murat Celik ◽  
Ayse Alp ◽  
Recep Dokuyucu ◽  
Ebru Zemheri ◽  
Seyma Ozkanli ◽  
...  
Keyword(s):  
Caffeic Acid ◽  
Supportive Therapy ◽  
Mitotic Cell ◽  
Caffeic Acid Phenethyl Ester ◽  
Stress Index ◽  
Control Group ◽  
Albino Rats ◽  
Immune Reactivity ◽  
Protective Effects ◽  
Cell Counts

The protective effects of Caffeic Acid Phenethyl Ester (CAPE) and intralipid (IL) on nephrotoxicity caused by acute Dichlorvos (D) toxicity were investigated in this study. Forty-eight Wistar Albino rats were divided into 7 groups as follows: Control, D, CAPE, intralipid, D + CAPE, D + IL, and D + CAPE + IL. When compared to D group, the oxidative stress index (OSI) values were significantly lower in Control, CAPE, and D + IL + CAPE groups. When compared to D + IL + CAPE group, the TOS and OSI values were significantly higher in D group (P<0.05). When mitotic cell counts were assessed in the renal tissues, it was found that mitotic cell count was significantly higher in the D group while it was lower in the D + CAPE, D + IL, and D + IL + CAPE groups when compared to the control group (P<0.05). Also, immune reactivity showed increased apoptosis in D group and low profile of apoptosis in the D + CAPE group when compared to the Control group. The apoptosis level was significantly lower in D + IL + CAPE compared to D group (P<0.05) in the kidneys. As a result, we concluded that Dichlorvos can be used either alone or in combination with CAPE and IL as supportive therapy or as facilitator for the therapeutic effect of the routine treatment in the patients presenting with pesticide poisoning.

The Protective Effects of Caffeic Acid Phenethyl Ester on Acetylsalicylic Acid-induced Lung Injury in Rats

2016 ◽  
Vol 29 (6) ◽  
pp. 328-334 ◽  
Author(s):  
Mahşuk Taylan ◽  
Halide Kaya ◽  
Melike Demir ◽  
Osman Evliyaoğlu ◽  
Hadice Selimoglu Sen ◽  
...  
Keyword(s):  
Lung Injury ◽  
Acetylsalicylic Acid ◽  
Caffeic Acid ◽  
Caffeic Acid Phenethyl Ester ◽  
Protective Effects

scholarly journals Sphingolipids as a Novel Therapeutic Target in Radiation-Induced Lung Injury

2021 ◽  
Author(s):  
Jeffrey R. Jacobson
Keyword(s):  
Lung Injury ◽  
Cell Injury ◽  
Inflammatory Responses ◽  
Small Animal ◽  
Protective Effects ◽  
Sphingosine 1 Phosphate ◽  
Radiation Induced ◽  
Injury Models

AbstractRadiation-induced lung injury (RILI) is a potential complication of thoracic radiotherapy that can result in pneumonitis or pulmonary fibrosis and is associated with significant morbidity and mortality. The pathobiology of RILI is complex and includes the generation of free radicals and DNA damage that precipitate oxidative stress, endothelial cell (EC), and epithelial cell injury and inflammation. While the cellular events involved continue to be elucidated and characterized, targeted and effective therapies for RILI remain elusive. Sphingolipids are known to mediate EC function including many of the cell signaling events associated with the elaboration of RILI. Sphingosine-1-phosphate (S1P) and S1P analogs enhance EC barrier function in vitro and have demonstrated significant protective effects in vivo in a variety of acute lung injury models including RILI. Similarly, statin drugs that have pleiotropic effects that include upregulation of EC S1P receptor 1 (S1PR1) have been found to be strongly protective in a small animal RILI model. Thus, targeting of EC sphingosine signaling, either directly or indirectly, to augment EC function and thereby attenuate EC permeability and inflammatory responses, represents a novel and promising therapeutic strategy for the prevention or treatment of RILI.

Protective effects of caffeic acid phenethyl ester against acute radiation-induced hepatic injury in rats

2015 ◽  
Vol 39 (2) ◽  
pp. 683-689 ◽  
Author(s):  
JianJun Chu ◽  
Xiaojun Zhang ◽  
Liugen Jin ◽  
Junliang Chen ◽  
Bin Du ◽  
...  
Keyword(s):  
Caffeic Acid ◽  
Hepatic Injury ◽  
Caffeic Acid Phenethyl Ester ◽  
Acute Radiation ◽  
Protective Effects ◽  
Radiation Induced

scholarly journals Protective effects of dehydroepiandrosterone (DHEA) vs caffeic acid phenethyl ester (CAPE) against ischemia-reperfusion injury in rat ovary

2020 ◽  
Vol 7 (1) ◽  
pp. 384-389
Author(s):  
Ali Doğukan Angın ◽  
Önder Sakin ◽  
Muzaffer Seyhan Cıkman ◽  
İsmet Gün ◽  
Ramazan Denizli ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Caffeic Acid ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Caffeic Acid Phenethyl Ester ◽  
Ovarian Torsion ◽  
Albino Rats ◽  
Protective Effects ◽  
Primordial Follicles ◽  
The Third

Objective: In this study, the effectiveness of caffeic acid phenethyl ester (CAPE) and Dehydroepiandrosterone (DHEA) in preventing ischemia reperfusion injury associated with ovarian torsion have been investigated. Materials and Methods: Twenty four adult female Wistar Albino rats were randomly divided into four groups. Ovaries were not twisted, and only healthy ovarian tissues were removed from the rats in the first group, while ovaries were twisted for 3 hours in the other groups. The second group did not receive any medications before the ovaries were untwisted, while 20 micromole/kg of CAPE was applied on peritoneal surface to the third group, and 60 mg/kg of DHEA was administered intraperitoneally to the fourth group. Results: The level of primordial follicles was higher in the third group compared to the second group after the torsion of the ovary (p=0.017). The mean level of primary follicles was higher in the first group compared to the number of follicles in the third and fourth groups after the torsion of the ovary (p<0.001). The median hemorrhage level was higher in the second group following ovarian torsion compared to that in the first group (p=0.005). Conclusion: Agents that have been considered to reduce injury resulting from ischemia-reperfusion proved ineffective during the early stages in terms of the number of follicles in the ovaries; however, we believe that long-term studies may be more beneficial.

scholarly journals Protectin conjugates in tissue regeneration 1 restores lipopolysaccharide-induced pulmonary endothelial glycocalyx loss via ALX/SIRT1/NF-kappa B axis

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Xin-Yang Wang ◽  
Xin-Yu Li ◽  
Cheng-Hua Wu ◽  
Yu Hao ◽  
Pan-Han Fu ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Inflammatory Cytokines ◽  
Tissue Regeneration ◽  
Umbilical Vein ◽  
Endothelial Glycocalyx ◽  
Lipid Mediator ◽  
Protective Effects ◽  
Pulmonary Vascular Permeability

Abstract Background Endothelial glycocalyx loss is integral to increased pulmonary vascular permeability in sepsis-related acute lung injury. Protectin conjugates in tissue regeneration 1 (PCTR1) is a novel macrophage-derived lipid mediator exhibiting potential anti-inflammatory and pro-resolving benefits. Methods PCTR1 was administrated intraperitoneally with 100 ng/mouse after lipopolysaccharide (LPS) challenged. Survival rate and lung function were used to evaluate the protective effects of PCTR1. Lung inflammation response was observed by morphology and inflammatory cytokines level. Endothelial glycocalyx and its related key enzymes were measured by immunofluorescence, ELISA, and Western blot. Afterward, related-pathways inhibitors were used to identify the mechanism of endothelial glycocalyx response to PCTR1 in mice and human umbilical vein endothelial cells (HUVECs) after LPS administration. Results In vivo, we show that PCTR1 protects mice against lipopolysaccharide (LPS)-induced sepsis, as shown by enhanced the survival and pulmonary function, decreased the inflammatory response in lungs and peripheral levels of inflammatory cytokines such as tumor necrosis factor-α, interleukin-6, and interleukin-1β. Moreover, PCTR1 restored lung vascular glycocalyx and reduced serum heparin sulphate (HS), syndecan-1 (SDC-1), and hyaluronic acid (HA) levels. Furthermore, we found that PCTR1 downregulated heparanase (HPA) expression to inhibit glycocalyx degradation and upregulated exostosin-1 (EXT-1) protein expression to promote glycocalyx reconstitution. Besides, we observed that BAY11-7082 blocked glycocalyx loss induced by LPS in vivo and in vitro, and BOC-2 (ALX antagonist) or EX527 (SIRT1 inhibitor) abolished the restoration of HS in response to PCTR1. Conclusion PCTR1 protects endothelial glycocalyx via ALX receptor by regulating SIRT1/NF-κB pathway, suggesting PCTR1 may be a significant therapeutic target for sepsis-related acute lung injury.

AB0162 Protective Effects of Caffeic Acid Phenethyl Ester (CAPE) on Cyclophosphamide Induced Hemorrhagic Cystitis in Rats

2015 ◽  
Vol 74 (Suppl 2) ◽  
pp. 944.4-945
Author(s):  
E. Uysal ◽  
H.R. Yılmaz ◽  
Y. Ugan ◽  
A. Altuntas ◽  
A. Doğru ◽  
...  
Keyword(s):  
Caffeic Acid ◽  
Hemorrhagic Cystitis ◽  
Caffeic Acid Phenethyl Ester ◽  
Protective Effects

Formulation development of folic acid conjugated PLGA nanoparticles for improved cytotoxicity of Caffeic acid phenethyl ester

2021 ◽  
Vol 09 ◽  
Author(s):  
Harshad S Kapare ◽  
Sathiyanarayanan L ◽  
Arulmozhi S ◽  
Kakasaheb Mahadik
Keyword(s):  
Folic Acid ◽  
Drug Release ◽  
Caffeic Acid ◽  
Caffeic Acid Phenethyl Ester ◽  
Therapeutic Effects ◽  
Formulation Development ◽  
Sustained Drug Release ◽  
Active Constituent

Background: Honey bee propolis is one of the natural product reported in various traditional systems of medicines including Ayurveda. Caffeic acid phenethyl ester (CAPE) is an active constituent of propolis which is well known for its anticancer potential. The therapeutic effects of CAPE are restricted owing to its less aqueous solubility and low bioavailability. Objective: In this study CAPE loaded folic acid conjugated nanoparticle system (CLFPN) was investigated to enhance solubility, achieve sustained drug release and improved cytotoxicity of CAPE. Methods: Formulation development, characterization and optimization were carried out by design of experiment approach. In vitro and in vivo cytotoxicity study was carried out for optimized formulations. Results: Developed nanoparticles showed particle size and encapsulation efficiency of 170 ± 2 - 195 ± 3 nm and 75.66 ± 1.52 - 78.80 ± 1.25 % respectively. Optimized formulation CLFPN showed sustained drug release over a period of 42 h. GI50 concentration was decreased by 46.09% for formulation as compared to CAPE in MCF-7 cells indicating targeting effect of CLFPN. An improved in vitro cytotoxic effect was reflected in in-vivo Daltons Ascites Lymphoma model by reducing tumor cells count. Conclusion: The desired nanoparticle characteristic with improved in vivo and in vitro cytotoxicity was shown by developed formulation. Thus it can be further investigated for biomedical applications.

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