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[Comparison of the in vitro activities of ammonium humate and of enzymically oxidized chlorogenic and caffeic acids against type 1 and type 2 human herpes virus (author's transl)].

Ammonium humate (prepared from marsh water humic acids) as well as enzymically oxidized diphenolic compounds such as the oxidation products of chlorogenic and caffeic acids have strong antiviral activities in vitro. The effective concentrations lie considerably outside the cytotoxic range of the compounds mentioned.

Adsorption↗

Antiarrhythmic effect of caffeic acid phenethyl ester (CAPE) on myocardial ischemia/reperfusion injury in rats.

OBJECTIVES: The present study was designed to determine the antiarrhythmic effect of caffeic acid phenethyl ester (CAPE), an active component of propolis, which exhibits antioxidant properties, in rats subjected to myocardial ischemia and ischemia-reperfusion (I/R) injury. DESIGN AND METHODS: Rats were subjected to 30 min coronary artery occlusion for evaluating the effect of CAPE on the myocardial ischemia injury. While in the myocardial I/R injury study, the coronary artery was ligated for a 5-min period of ischemia followed by a 30-min period of reperfusion. Animals were pretreated with or without CAPE before coronary artery ligation and the severity of myocardial ischemia- and I/R-induced arrhythmias and mortality were compared. RESULTS: Pretreatment of CAPE (0.1 and 1 microg/kg) not only reduced both the incidence and duration of ventricular tachycardia (VT) and ventricular fibrillation (VF) but also decreased the mortality during the myocardial ischemia and I/R injury period. CONCLUSIONS: Our results suggest that CAPE is a potent antiarrhythmic agent with cardioprotective effects in myocardial ischemia and I/R injury rats.

Animals↗

Inhibitory effects of caffeic acid phenethyl ester on cancer cell metastasis mediated by the down-regulation of matrix metalloproteinase expression in human HT1080 fibrosarcoma cells.

Caffeic acid phenethyl ester (CAPE) derived from honeybee propolis has been used as a folk medicine. Recent study also revealed that CAPE has several biological activities including antioxidation, anti-inflammation and inhibition of tumor growth. The present study investigated the effect of CAPE on tumor invasion and metastasis by determining the regulation of matrix metalloproteinases (MMPs). Matrix metalloproteinases, which are zinc-dependent proteolytic enzymes, play a pivotal role in tumor metastasis by cleavage of extracellular matrix (ECM) as well as nonmatrix substrates. On this line, we examined the influence of CAPE on the gene expression of MMPs (MMP-2, MMP-9, MT1-MMP), tissue inhibitor of metalloproteinase-2 (TIMP-2) and in vitro invasiveness of human fibrosarcoma cells. Dose-dependent decreases in MMP and TIMP-2 mRNA levels were observed in CAPE-treated HT1080 human fibrosarcoma cells as detected by reverse transcriptase-polymerase chain reaction (RT-PCR). Gelatin zymography analysis also exhibited a significant down-regulation of MMP-2 and MMP-9 expression in HT1080 cells treated with CAPE compared to controls. In addition, CAPE inhibited the activated MMP-2 activity as well as invasion, motility, cell migration and colony formation of tumor cells. These data therefore provide direct evidence for the role of CAPE as a potent antimetastatic agent, which can markedly inhibit the metastatic and invasive capacity of malignant cells.

Caffeic Acids↗

Oxidative stress in testicular tissues of rats exposed to cigarette smoke and protective effects of caffeic acid phenethyl ester.

AIM: To show the oxidative stress after cigarette smoke exposure in rat testis and to evaluate the effects of caffeic acid phenethyl ester (CAPE). METHODS: Twenty-one rats were divided into three groups of seven. Animals in Group I were used as control. Rats in Group II were exposed to cigarette smoke only (4 x 30 min/d) and rats in Group III were exposed to cigarette smoke and received daily intraperitoneal injections of CAPE (10 micromol/kg x d). After 60 days all the rats were killed and the levels of nitric oxide (NO) and anti-oxidant enzymes such as superoxide-dismutase, catalase and glutathione peroxidase (GSH-Px) and the level of malondialdehyde were studied in the testicular tissues of rats with spectrophotometric analysis. RESULTS: There was a significant increase in catalase and superoxide-dismutase activities in Group II when compared to the controls, but the levels of both decreased after CAPE administration in Group III. GSH-Px activity was decreased in Group II but CAPE caused an elevation in GSH-Px activity in Group III. The difference between the levels of GSH-Px in Group I and Group II was significant, but the difference between groups II and III was not significant. Elevation of malondialdehyde after smoke exposure was significant and CAPE caused a decrease to a level which was not statistically different to the control group. A significantly increased level of NO after exposure to smoke was reversed by CAPE administration and the difference between NO levels in groups I and III was statistically insignificant. CONCLUSION: Exposure to cigarette smoke causes changes in the oxidative enzyme levels in rat testis, but CAPE can reverse these harmful effects.

Animals↗

Does propofol or caffeic acid phenethyl ester prevent lung injury after hindlimb ischaemia-reperfusion in ventilated rats?

BACKGROUND: To investigate the effects of propofol and caffeic acid phenethyl ester (CAPE) on prevention of lung injury as a remote organ after performing hindlimb ischaemia-reperfusion (IR) in a rat model. METHODS: The animals were divided randomly into one of four groups: sham, no IR (n = 8), control, IR, (n = 8), CAPE group, IR with CAPE, (n = 8), propofol group, IR with P, (n = 8). After the rats were anaesthetised, the animals in the CAPE group received CAPE of 10 micromol, in the propofol group received propofol 50 mg/kg, in the control group received a similar volume of saline solution by means of intraperitoneal injection 1 h before reperfusion. After 4 h of ischaemia the tourniquet was removed and the animals were released for reperfusion for 4 h thereafter. At the end of the reperfusion period, a median sternotomy was performed. A blood sample was obtained for plasma malondialdehyde (MDA). The lung tissues were also removed for MDA assays, myeloperoxidase (MPO) activity, and histopathological examination. RESULTS: Plasma and lung MDA levels, and lung MPO activity were significantly higher in the control group compared to the other groups (p < 0.0005). In the CAPE group, these were significantly lower compared to the control group (p < 0.0005). Also, propofol caused a marked reduction in the MDA levels and MPO activity compared with control group (p < 0.0005), with no significant difference compared to that of the sham group. Histopathologically, the scores resulted in a grade zero (8/8) in the sham group, 3 (3/8) or 4 (5/8) in the control group, 1 (2/8) or 2 (6/8) in the CAPE group, and 1 (3/8) or 2 (5/8) in the propofol group. CONCLUSION: Propofol and CAPE seem to be effective in protecting against lung injury caused by increased oxidative stress and neutrophil accumulation after hindlimb IR in a rat model.

Animals↗

Inhibitory effects of caffeic acid phenethyl ester analogues on experimental lung metastasis of murine colon 26-L5 carcinoma cells.

We have previously examined the antiproliferative activity of caffeic acid phenethyl ester (CAPE) and its 20 analogues against six tumor cell lines, and found that CAPE analogues possess selective antiproliferative activity toward the murine colon 26-L5 carcinoma cell line. To extend our study, the effects of CAPE analogues on the metastatic development of murine colon 26-L5 carcinoma cells in the lung were examined. The oral administration of CAPE (5 mg/mice/d) for 7 d after tumor inoculation decreased the tumor weight and the number of tumor nodules in the lung by 50% and 50%, respectively, compared to the control, while CAPE (5 mg/mice/d) administered for 7 d before tumor inoculation showed no significant effect. Besides CAPE, 4-phenylbutyl caffeate, 8-phenyl-7-octenyl caffeate, 2-cyclohexylethyl caffeate and n-octyl caffeate at an oral dose of 2 mg/mice/d caused a 55%, 43%, 55% and 35% reduction of the tumor nodules in their lung metastasis formation, respectively. These results further elaborate the possibility of CAPE and its analogues to become a new class of chemopreventive agents for the treatment of colon cancer metastasis.

Administration, Oral↗

Retention of caffeic acid derivatives in dried Echinacea purpurea.

Different drying methods were applied to fresh Canadian-grown Echinacea purpurea flowers to determine optimal drying procedures for preserving caffeic acid derivatives. Fresh flowers of E. purpurea were dried by freeze-drying (FD), vacuum microwave drying with full vacuum (VMD), and air-drying (AD) at 25, 40, and 70 degrees C. Using HPLC, chicoric acid and caftaric acid levels were quantitated in dried flowers. These acids were significantly affected by the drying method conditions used. Although significant (p < 0.05) loss of chicoric acid was observed when flowers were stored at high moisture, VMD flowers with a low moisture content retained the highest levels of chicoric acid and caftaric acid similar to FD flowers. Flowers that were AD at 25 degrees C retained about 50%, while those dried by AD at 70 degrees C resulted in the lowest retention of these acids. Although flowers dried by AD at 40 degrees C retained relatively high amounts of chicoric acid and caftaric acid, the time (55 h) required to reach optimal drying was considerably longer than that (47 min) for VMD.

Caffeic Acids↗

Caffeic acid phenethyl ester prevents intestinal reperfusion injury in rats.

BACKGROUND/PURPOSE: Ischemia-reperfusion injury is encountered frequently in conditions that diminish intestinal blood flow. Caffeic acid phenethyl ester (CAPE), which is a specific component of the honeybee hive product propolis, exhibits potential antioxidant properties. This experimental study was designed to determine the effect of CAPE on ischemia-reperfusion injury in rat intestine. METHODS: Fifty rats were divided into 5 groups; sham (SH), saline ischemia (SI), saline reperfusion (SR), CAPE ischemia (CI), and CAPE reperfusion (CR). Either CAPE, 10 micromol/kg, or saline was administered intraperitoneally 30 minutes before ischemia. Intestinal ischemia for 30 minutes and reperfusion for 60 minutes were applied. Ileum specimens were obtained to determine the tissue levels of malondialdehyde, superoxide dismutase, catalase, and histological changes. RESULTS: Malondialdehyde levels in the CR group did not increase after reperfusion when compared with the CI group. However, statistically significant differences were observed between the SR and SI groups. Additional mucosal injury in the CR group when compared with the CI group was not observed. Whereas, there was a statistically significant increase in mucosal injury in the SR group. Reperfusion did not cause further injuries through both biochemical and histological parameters in the CR group. CONCLUSIONS: Results of this study showed that prophylactic administration of CAPE in ischemic condition prevents reperfusion injuries by eliminating oxygen radicals and inhibiting polymorphonuclear leukocyte infiltration. CAPE may be useful in combating the diseases of oxidative stress.

Animals↗

Caffeic acid phenethyl ester inhibits T-cell activation by targeting both nuclear factor of activated T-cells and NF-kappaB transcription factors.

Caffeic acid phenethyl ester (CAPE), which is derived from the propolis of honeybee hives, has been shown to reveal anti-inflammatory properties. Since T-cells play a key role in the onset of several inflammatory diseases, we have evaluated the immunosuppressive activity of CAPE in human T-cells, discovering that this phenolic compound is a potent inhibitor of early and late events in T-cell receptor-mediated T-cell activation. Moreover, we found that CAPE specifically inhibited both interleukin (IL)-2 gene transcription and IL-2 synthesis in stimulated T-cells. To further characterize the inhibitory mechanisms of CAPE at the transcriptional level, we examined the DNA binding and transcriptional activities of nuclear factor (NF)-kappaB, nuclear factor of activated cells (NFAT), and activator protein-1 (AP-1) transcription factors in Jurkat cells. We found that CAPE inhibited NF-kappaB-dependent transcriptional activity without affecting the degradation of the cytoplasmic NF-kappaB inhibitory protein, IkappaBalpha. However, both NF-kappaB binding to DNA and transcriptional activity of a Gal4-p65 hybrid protein were clearly prevented in CAPE-treated Jurkat cells. Moreover, CAPE inhibited both the DNA-binding and transcriptional activity of NFAT, a result that correlated with its ability to inhibit phorbol 12-myristate 13-acetate plus ionomycin-induced NFAT1 dephosphorylation. These findings provide new insights into the molecular mechanisms involved in the immunomodulatory and anti-inflammatory activities of this natural compound.

Caffeic Acids↗

The effects of caffeic acid phenethyl ester on tissue damage in lung after hindlimb ischemia-reperfusion.

AIM: The aim of this study was to investigate the effects of caffeic acid phenethyl ester (CAPE) on the lungs as a remote organ after performing hindlimb ischemia-reperfusion (I/R) and by assessing biochemical and histopathological analysis. METHODS: The animals were divided into three groups: control, I/R, and I/R with CAPE. I/R period for 8 h was performed on the right hindlimb of all the anesthesied rats in I/R and CAPE with I/R group. In the CAPE with I/R group, the animals received CAPE 10 microM by intraperitoneal injection 1h before the reperfusion. The animals in the control and I/R groups received a similar volume of saline solution by means of intraperitoneal injection. At the end of the reperfusion period, a midsternotomy was performed. Blood, bronchoalveolar lavage (BAL) and lung tissue were obtained, and were used for biochemical and histopathological examination. RESULTS: The tissue and serum malondyaldehyde levels were significantly lower in the control (P=0.0001 and 0.001, respectively) and in the CAPE with I/R groups (P=0.0001 and 0.003, respectively) compared to the I/R group. Tissue Na(+)-K(+) ATPase activity in the CAPE with I/R group was significantly higher than in the I/R group (P=0.0001). Reduced activity was found in the I/R group compared to the control group (P=0.0001). Myeloperoxidase activity (P=0.001) and protein concentration (P=0.034) in BAL were significantly reduced in CAPE-treated animals when compared with the I/R group. A decreased activity and protein concentration were found in the control group compared to the I/R group (P=0.0001 and 0.024, respectively). The lungs of the I/R group displayed intense peribronchial and perivascular leukocytic infiltration in histopathological examination compared to the CAPE with I/R group (P<0.05). CONCLUSION: CAPE seems to be effective in protecting remote organ injury caused by increased oxidative stress and neutrophil accumulation that results from an I/R injury.

Animals↗

Protective effect of caffeic acid phenethyl ester (CAPE) on lipid peroxidation and antioxidant enzymes in diabetic rat liver.

The aim of this study was to examine the effect of caffeic acid phenethyl ester (CAPE) on lipid peroxidation (LPO) and the activities of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) in the liver of streptozotocin (STZ)-induced diabetic rats. Twenty-seven rats were randomly divided into three groups: group I, control non-diabetic rats (n = 9); group II, STZ-induced, untreated diabetic rats (n = 8); group III, STZ-induced, CAPE-treated diabetic rats (n = 10), which were intraperitoneally injected with CAPE (10 microM kg(-1) day(-1)) after 3 days followed by STZ treatment. The liver was excised after 8 weeks of CAPE treatment, the levels of malondialdehyde (MDA) and the activities of SOD, CAT, and GSH-Px in the hepatic tissues of all groups were analyzed. In the untreated diabetic rats, MDA markedly increased in the hepatic tissue compared with the control rats (p < 0.0001). However, MDA levels were reduced to the control level by CAPE. The activities of SOD, CAT, and GSH-Px in the untreated diabetic group were higher than that in the control group (p < 0.0001). The activities of SOD and GSH-Px in the CAPE-treated diabetic group were higher than that in the control group (respectively, p < 0.0001, p < 0.035). There were no significant differences in the activity of CAT between the rats of CAPE-treated diabetic and control groups. Rats in the CAPE-treated diabetic group had reduced activities of SOD and CAT in comparison with the rats of untreated diabetic group (p < 0.0001). There were no significant differences in the activity of GSH-Px between the rats of untreated diabetic and CAPE-treated groups. It is likely that STZ-induced diabetes caused liver damage. In addition, LPO may be one of the molecular mechanisms involved in STZ-induced diabetic damage. CAPE can reduce LPO caused by STZ-induced diabetes.

Animals↗

Therapeutic effect of (E)-5-(2-bromovinyl)-2'-deoxyuridine, caffeic acid oxidation product, and trisodiumphosphonoformate on cutaneous herpes simplex virus type 1 infection in guinea pigs.

The influence of (E)-5-(2-bromovinyl)-2'-deoxyuridine (BVDU), caffeic acid oxidation product (KOP), and trisodiumphosphonoformate (TPF) on the course of the primary cutaneous herpes simplex virus infection was investigated by means of a guinea pig test model. The antiviral substances were applied in an ointment with 10% urea as a penetration mediator. When the treatment was initiated 15 minutes after virus inoculation, 3% BVDU effectively inhibited the development of herpetic vesicles and 0.1% BVDU prevented the appearance of herpetic satellites. Under the same conditions 1% and 3% KOP ointments inhibited the appearance of satellites; and 0.5% TPF ointment completely inhibited the development of cutaneous herpes lesions. Prophylactic drug administration given 24, 20, and 4 hours before virus inoculation was without any protective effect.

Animals↗

Role of caffeic acid phenethyl ester, an active component of propolis, against NAOH-induced esophageal burns in rats.

OBJECTIVES: This study was evaluated to investigate the efficacy of caffeic acid phenethyl ester (CAPE), which is a natural honeybee product exhibits a spectrum of biological activities including anti-microbial, anti-inflammatory, antioxidant and anti-tumoral actions, on the prevention of stricture development after esophageal caustic injuries in the rat. METHODS: Thirty healthy male Wistar albino rats were utilized in this study. The rats were randomly allotted into one of three experimental groups: group A (sham) animals were uninjured. Caustic esophageal burn was created by applying 1 ml 37.5% NaOH to the distal esophagus. Group B rats were injured but untreated. Group C rats were injured and received CAPE (10 micromol/kg/day i.p. for 28 days). Efficacy of the treatment was assessed by measuring the esophageal transit time, stenosis index, histopathologic damage score and biochemically by determining tissue hydroxyproline content, lipid peroxidation and antioxidant enzyme activities. RESULTS: The esophageal transit time, the stenosis index, histopathologic damage score and the hydroxyproline level were significantly increased in the untreated group compared with the sham and CAPE-treated groups. Treatment with CAPE decreased tissue hydroxyproline levels, histological damage, and the stenosis index, but except the esophageal transit time. Caustic esophageal burn also increased the lipid peroxidation and decreased the antioxidant enzyme activities in the untreated group. CAPE treatments decreased the elevated lipid peroxidation and also increased the reduced antioxidant enzyme activities. In corrosive esophageal burn group with no treatment, the most consistent findings were degenerative changes and increased in submucosal collagen content, and the luminal narrowing. CAPE treatment protected esophagus. Nevertheless, there was the slight increase in submucosal collagen. CONCLUSIONS: It is concluded that CAPE has a preventive effect on the stricture development after esophageal caustic injuries in the rat.

Animals↗

Effect of a propolis extract and caffeic acid phenethyl ester on formation of aberrant crypt foci and tumors in the rat colon.

We have studied the effect of propolis and its main active ingredient caffeic acid phenetyl ester (CAPE) on formation of aberrant crypt foci (ACF) and tumors in the rat colon in vivo. CAPE (50 mg/kg i.p.) reduced the formation of ACF and tumor induced by azoxymethane, while propolis ethanolic extract was without effect. These results suggest a potential anti-carcinogenesis of CAPE but not propolis.

Animals↗

Effect of caffeic acid phenethyl ester on cartilage in experimental osteoarthritis.

Activation of nuclear factor kappa B (NF-kappaBeta) in synovial cells is seen in RA and OA patients. Caffeic acid phenethyl ester (CAPE) is a specific and potent inhibitor of NF-kappaBeta. We aimed to determine the in vivo effects of intra-articular injections of CAPE on cartilage in an experimental rabbit osteoarthritis (OA) model. Two groups of six New Zealand white rabbits underwent unilateral anterior cruciate ligament transection (ACLT). Four weeks after ACLT, the test group was injected with 150 micro g/kg CAPE in 0.5% ethanol once daily for 2 weeks and the control group was injected the same amount of 0.5% ethanol intra-articularly. All rabbits were killed 2 weeks after the last injection, and cartilage tissue was evaluated morphologically. A histological score totaling 7 points was determined for each knee. The CAPE group showed significantly decreased cartilage destruction and reduced loss of matrix proteoglycans. The histological score for cartilage tissue was significantly better in the CAPE group than in the control group (3.0+/-0.25 vs 5.3+/-0.55, P=0.005). This study suggests that intra-articular injection of CAPE may protect cartilage against the development of experimentally induced OA.

Animals↗

Effect of caffeic acid phenethyl ester on proliferation and apoptosis of hepatic stellate cells in vitro.

AIM: To investigate the role of nuclear factor-kappaB (NF-kappaB) inhibitor caffeic acid phenethy1 ester (CAPE) in the proliferation, collagen synthesis and apoptosis of hepatic stellate cells (HSCs) of rats. METHODS: The HSCs from rats were isolated and cultured in Dulbecco's Modified Eagle's Medium (DMEM) and treated with CAPE. The proliferation and collagen synthesis of HSCs were determined by (3)H-TdR and (3)H-proline incorporation respectively, and the expression of type I, III procollagen genes was further explored by in situ hybridization. Apoptosis cell indices (AIs) were examined using terminal deoxynucleotidyl transferase- mediated DIG-dUTP nick end labeling (TUNEL). RESULTS: In activated HSC in culture, CAPE significantly inhibited (3)H-TdR and (3)H-proline incorporation by HSCs at concentrations of 5 micromol/L and 10 micromol/L respectively. CAPE also reduced the type I procollagen gene expression (P<0.05) at higher concentration. Apoptosis of HSC was induced by CAPE and the AIs were time-and dose-dependently increased from 2.82+/-0.73 % to 7.66+/-1.25 % at 12 h (P<0.01) and from 3.15+/-0.88 % to 10.61+/-2.88 % at 24 h (P<0.01). CONCLUSION: CAPE inhibits proliferation and collagen synthesis of HSC at lower concentration and induces HSC apoptosis at higher concentration.

Animals↗

Growth suppression and toxicity induced by caffeic acid phenethyl ester (CAPE) in type 5 adenovirus-transformed rat embryo cells correlate directly with transformation progression.

The active component of the honeybee hive product propolis, caffeic acid phenethyl ester (CAPE), induces a selective growth suppressive and toxic effect toward cloned rat embryo fibroblast cells transformed by adenovirus type 5 (Ad5) or the Ad5 E1A transforming gene versus untransformed cloned rat embryo fibroblast cells (Z-z. Su et al., Mol. Carcinog., 4: 231-242, 1991). The present study was conducted to determine whether CAPE-induced growth suppression/toxicity was a direct result of expression of the Ad5 E1A and E1B transforming genes or a consequence of the action of these genes resulting in the transformed state. For this investigation we used somatic cell hybrids and 5-azacytidine-treated Ad5-transformed rat embryo cells that display different stages of expression of the transformed phenotype. This series of cell lines has permitted us to determine whether expression of the transformed state and the stage of transformation progression regulates CAPE sensitivity. Evidence is presented indicating that sensitivity to CAPE is directly determined by the state of expression of the transformed progression phenotype, as opposed to simply the expression of the Ad5 E1A and E1B transforming genes. These results provide further evidence that CAPE may represent a unique compound that can specifically target progressed transformed cells for growth suppression and toxicity. An understanding of the mechanism underlying this selective effect of CAPE could result in the identification of important biochemical pathways mediating cellular transformation and progression of the transformed state.

Adenovirus E1A Proteins↗

Effect of caffeic acid phenethyl ester on treatment of experimentally induced methicillin-resistant Staphylococcus epidermidis endophthalmitis in a rabbit model.

This study investigated the anti-inflammatory effects of caffeic acid phenethyl ester (CAPE), a natural bee-produced compound, and compared it with corticosteroids in the treatment of experimentally induced methicillin-resistant Staphylococcus epidermidis (MRSE) endophthalmitis in addition to intravitreal antibiotics. An experimental endophthalmitis model was produced in 24 New Zealand albino rabbits by unilateral intravitreal injection of 0.1 ml of 4.7 x 10(4) colony-forming units (CFU) methicillin-resistant S. epidermidis. The animals were then divided randomly into three treatment groups and a control group, group 1 (six rabbits), received only intravitreal vancomycin (1.0 mg/0.1 ml); group 2 (six rabbits), received both intravitreal vancomycin (1.0 mg/0.1 ml) and intravitreal dexamethasone (400 microg/0.1 ml) and group 3 (six rabbits), received both intravitreal vancomycin (1.0 mg/0.1 ml) and subtenon CAPE (10 mg/0.3 ml) after 24 h post-infection. No treatment was given to the control group. Treatment efficacy was assessed by clinical examination, vitreous culture and histopathology. There were no statististically significant differences between clinical scores of all groups in examinations at 24 and 48 h post-infection (p = 0.915 and p = 0.067 respectively), but in examinations at 72 h post-infection and after 7 days post-infection, although the clinical scores of treatment groups were not significantly different from each other, they were significantly lower than the control group (p < 0.05). The culture results of all groups were sterile. As a result, CAPE was found to be as effective as dexamethasone in reducing inflammation in the treatment of experimental MRSE endophthalmitis when used with antibiotics. More studies are needed to determine the optimal administration route and effective dosage of this compound.

Analysis of Variance↗