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Aim: Scalp hairs are mainly innervated by sensitive fibers of trigeminal nerves. Ischemic neurodegeneration of trigeminal ganglion can cause denervation injury of scalp hairs. We investigated if there is a relationship between the degenerated neuron densities of trigeminal ganglion neuron densities and the numbers of degenerated hair follicles numbers following subarachnoid hemorrhage (SAH). Material and Method: Five normal (n=5), five SHAM (n=5), and ten (n=10) male rabbits were chosen from formerly experimental SAH created by cisternal homologous blood injection (0.75cc) group, which followed for three weeks. Degenerated neuron numbers of trigeminal ganglion and atrophic hair follicles numbers in the frontal areas of the scalp were examined by stereological methods. Degenerated neuron densities of trigeminal ganglions and atrophic hair follicles numbers were analyzed by the Mann-Whitney U test. Results: The mean degenerated neuron densities trigeminal ganglions (n/mm3) and atrophic hair follicles (n/mm2) were determined as 5±2/m3 and12±4/mm2 in control; 12±3/m3 and 41±8/mm2 in Sham and, 168±23/m3 and 79±14/mm2 in the study group (p>0.001). In the post-hoc analysis, all groups differed significantly from each other. A linear association was observed between the degenerated neuron densities of trigeminal ganglions and atrophic hair follicles (r: 0.343, p: 0.007). Conclusion: Trigeminal ganglion neurodegeneration may be an essential factor in hair follicles atrophy after SAH, which has not been mentioned in the literature so far.

Objective: Although the neurophysical mechanism of subthalamic nucleus (STN) stimulation is still unclear, STN with decreasing electric field strength may be re-charged by battery. According to the law defined by Einstein, the unified electromagnetic field (UF) energy formed by the electrically charged Auerbach ganglia co-oscillating with bowel movements, can be transported by afferent nerves to charge the brain, like as battery. This study examines the rationality of the current theory.Methods: In this study, 18 rats with 360±20 gr weighted were divided into 3 groups according to their intestinal pulsation ranges as: 10±3/GI; 7±2/GII and 3±1/GIII. Auerbach's ganglia density (n/AG/mm3), Auerbach ganglia neuron density (n/AGN/mm3) were estimated by taking 0.5 mm sections at 10 mm intervals from 5 different distances from the midline of the ascending colon; and STN neuron densities (n/STN/mm3) were estimated. The Auerbach ganglia neurons -accepted as vibrating particles- numbers (VPN/mm3) estimated with: VPN=nAxnAG; the unified field strength (UFS) values formed by Auerbach's ganglia was estimated by UFS=fxVPN equation. UFS and n/STN values were compared Mann Witney U test. Results: VPN/UFS/nSTN values were: (13.345±2.143)/(11.146±1.689)/132.863±12.654 in GI; (11.762±1.843)/(8.434±1.119)/121.371±9.872 in GII and (8.659±903)/(7.109±768) /118.127±6942 in GIII) Statistical results between UFS/nSTN were found as: p, Amaç: Subtalamik çekirdek stimülasyonunun (STN) nörofiziksel mekanizması hala belirsiz olsa da, azalan elektrik alan gücü ile STN pil ile yeniden şarj edilebilir. Einstein'ın tanımladığı yasaya göre, elektrik yüklü Auerbach gangliyonlarının bağırsak hareketleriyle birlikte titreşerek oluşturduğu birleşik elektromanyetik alan (UF) enerjisi, afferent sinirler tarafından pil gibi beyni şarj etmek üzere taşınabilir. Bu çalışma, mevcut teorinin rasyonelliğini incelemektedir. Gereç ve Yöntem: Bu çalışmada 360±20 gr ağırlığındaki 18 rat, intestinal pulsasyon aralıklarına göre 10±3/GI; 7±2/GII ve 3±1/GIII olmak üzere 3 grubua bölündü. Çıkan kolon orta hattından 5 farklı mesafeden 10 mm aralıklarla 0,5 mm kesitler alınarak Auerbach ganglion yoğunluğu (n/AG/mm3), Auerbach ganglion nöron yoğunluğu (n/AGN/mm3) hesaplandı ve STN nöron yoğunlukları (n/STN/mm3) tahmin edildi. Titreşen parçacıklar olarak kabul edilen Auerbach ganglia nöronlarının sayıları (VPN/mm3), VPN=nAxnAG; Auerbach ganglionlarının oluşturduğu birleşik alan kuvveti (UFS) değerleri, UFS=fxVPN denklemi ile olacak şekilde tahmin edildi. UFS ve n/STN değerleri Mann Witney U testi ile karşılaştırıldı. Bulgular: VPN/UFS/nSTN değerleri: (13.345±2.143)/(11.146±1.689)/132.863±12.654 GI'de; (11.762±1.843)/(8.434±1.119)/121.371±9.872 GII'de ve (8.659±903)/(7.109±768) /118.127±6942 GIII'de) UFS/nSTN arasındaki istatistiksel sonuçlar: p

Adults with end-stage of chronic liver diseases have lower antibody titers after hepatitis-B vaccination. We have less amount of knowledge about the effect of non-viral cause chronic liver fibrosis on vaccination. In this study, we investigated the effect of non-viral chronic liver fibrosis on hepatitis B vaccine and the effect of tetanous toxoid co-administration at the level of humoral and cellular immune responses in an experimental model.Hepatitis B vaccine was administered either alone or in combination with tetanus toxoid in thioacetamide-induced fibrotic BALB/c mice. Fibrosis level was determined by Knodell scoring. Anti-HBsAg, biochemical parameters, inflammatory (IL-1β, TNF-α), and anti-inflammatory (IL-10) cytokine levels were investigated in serum samples by automated systems and ELISA; respectively. Frequencies of activated lymphocytes were determined in flow cytometer.Antibody titers significantly decreased after immunization of fibrotic mice. However, co-administration of toxoid significantly elevated antibody titer. The percentage of CD19Non-viral chronic liver fibrosis causes a reduction on specific antibody level after vaccination. Reduction on Breg cell frequency may have an effect on elevation of antibody level after co-administration of tetanus toxoid.

Surgical site infection is a challenging situation for all types of surgeons. Extensive debridement with or without implant removal can create soft tissue defects. A well-vascularized, adequate soft tissue is needed to cover the wound and to fill the dead space for proper healing. Herein, we describe our approach to a large posterior trunk defect with dead space and our solution to manage an intraoperative complication using a free-style deepithelialized propeller flap. WOS:000661415100035 PubMed: 34145835

Vascular endothelial growth factor-A (VEGF-A) gene expression in an experimental gentamicin-induced nephrotoxicity and ameliorative effect of caffeic acid phenethyl ester (CAPE) was investigated in rats. Animals were divided into four groups (n=8); control (C) group animals were given 10% dimethylsulfoxide (DMSO); gentamicin (G) group animals were given 100 mg/kg/day gentamicin; CAPE group animals were given 30 mg/kg/day CAPE and CAPE+G group animals were given 100 mg/kg/day gentamicin plus 30 mg/kg/day CAPE. Serum creatinine and BUN levels significantly increased in gentamicin group as compared to the control group (p0.05). Gene expression level of VEGF-A in gentamicin group significantly decreased as compared to the control group, however, CAPE treatment did not have any increasing effect on the gene expression level. According to histopathological investigation, gentamicin treatment caused prominent degeneration in kidney tissue and CAPE treatment had only slight beneficial effect on lowering the tissue degeneration. The results showed that gentamicin decreases VEGF-A gene expression and this might be related to the tissue degeneration at cellular level. However, CAPE treatment did not have significant ameliorative effect in lowering the gentamicin induced nephrotoxicity. [Med-Science 2018; 7(4.000): 805-9]

Investigation of the effect of Dexmedetomidine (Dex) on inflammatory bowel diseases (IBD) induced renal damage by using an experimental model. IBD frequently cause reduction in renal function and renal failure. Since perioperative anesthesia and postoperative conditions in intensive care can cause acute kidney injury and reduction on renal function; deciding on a sedative and anesthetic agent without side effects would reduce IBD caused renal damage. We investigated histopathological, electron microscopic analyzes and antioxidant effects of Dex on kidney tissue during trinitrobenzene sulfonic acid (TNBS) induced damage in BALB/c mice at two different concentrations of Dex; 5μg/kg and 30μg/kg. Blood samples were collected to analyze creatinine levels. The levels of malondialdehyde (MDA) and activity of antioxidant enzymes glutathione (GSH) and superoxide dismutase (SOD) were measured in tissue homogenates. Histopathological and ultrastructural changes in kidney following TNBS induction were significantly reduced in Dex treatment groups. Administration of Dex significantly reduced creatinine levels. MDA levels were significantly reduced in Dex groups. Administration of Dex brought back GSH level to control level. Administration of Dex significantly 1.48 and 1.96 times increased SOD activity at 5μg/kg and 30 μg/kg, respectively. Dexmedetomidine treatment may have benefits to prevent IBD induced renal damage. [Med-Science 2018; 7(3.000): 594-9]

Amaç: Vücudumuzdaki en büyük organ olan karaciğerin immün sistem üzerindeki etkisi tam olarak bilinmemektedir. Projemizin amacı, kronik karaciğer fibrozu esnasında karaciğer ve sekonder lenfoid organ olan dalakta gelişen hücresel yanıtın moleküler düzeyde analizi ve ayrıca genç ve yaşlı deneklerden elde edilen verilerin karşılaştırılarak yaşlanmanın karaciğerdeki immün yanıt üzerine etkisinin araştırılmasıdır. Materyal ve Metot: Kronik fibroz modeli oluşturmak amacıyla BALB/c farelere ip. Thioacetamide enjeksiyonu yapılmıştır. Tüm gruplarda karaciğer ve dalak dokularında inflamatuar ve anti-inflamatuar sitokin genlerinin ifade edilme düzeyleri araştırılmış, karaciğer dokularında histolojik ve immünohistokimyasal analizler yapılmıştır.Bulgular: Genç fibrotik deneklerin karaciğer dokularında TNF-IL-10 ve TGF- gen ifade düzeyleri genç naive deneklere göre artış gösterirken, ROR-t,ve IFN- gen ifade düzeylerinde azalma saptanmıştır. Dalak dokularında ise GATA-3, FOXP3 ve TNF- gen ifade düzeyleri artış göstermiştir. Yaşlı fibrotik deneklerin karaciğer dokularında ROR-t, T-bet, IL-10 ve IFN- gen ifadeleri yaşlı naive deneklere göre azalmaktadır. Dalakta ise T-bet ve IFN- gen ifade seviyeleri azalmıştır. Yaşlanma ile beraber karaciğer dokusunda T-bet, IL-10 ve TGF- gen ifadelerinde artış saptanmıştır. Ayrıca yaşlı deneklerin dalaklarında TGF-IL-17, ROR-t ve IL-2 dışındaki tüm genlerin ifade düzeyleri artmıştır. Sonuç: Karaciğer fibrozu esansında genç bireylerde karaciğerin hem inflamatuar hem de anti-inflamatuar yanıtı desteklediği, dalakta ise anti-inflamatuar yanıtı desteklediği anlaşılmaktadır. Yaşlanmaya bağlı olarak fibroza karşı verilen immün yanıtın farklılık gösterdiği anlaşılmaktadır.Anahtar kelimeler: Fibrozis, Karaciğer, Dalak, Sitokin Aim:The effect of the liver, the largest organ in our body, on the immune system is not fully known. The aim of our project is to analyze the cellular response that develops in the liver and the spleen, at molecular level during chronic liver fibrosis, and also to investigate the effect of aging on the immune response in the liver by comparing the data obtained from young and old subjects.Material and Method: In order to create chronic fibrosis model thioacetamide was injected via i.p route to BALB/c mice. The expression levels of inflammatory and anti-inflammatory cytokine genes in liver and spleen tissues were investigated in all groups, and histological and immunohistochemical analyzes were performed on liver tissues.Results: TNF-IL-10 and TGF- gene expression levels in liver tissues of young fibrotic subjects increased compared to young naive subjects, while ROR-t, IL-4 and IFN- gene expression levels decreased. GATA-3, FOXP3 and TNF- gene expression levels increased in spleen tissues. ROR-t, T-bet, IL-10 and IFN-gene expressions in the liver tissues of elderly fibrotic subjects decreased compared to elderly naive subjects. In the spleen, T-bet and IFN- gene expression levels decreased. T-bet, IL-10 and TGF- gene expressions increased in liver tissue as a result of aging. In addition, expression levels of all genes except TGF-IL-17, ROR-t and IL-2 increased in the spleens of elderly subjects. Conclusion: Our findings reveal that the liver supports both the inflammatory and anti-inflammatory response in young individuals during liver fibrosis, while the spleen supports the anti-inflammatory response. It appears that the immune response to fibrosis varies depending on aging.Key Words: Fibrosis, Liver, Spleen, Cytokine 107

Aim: Panel Reactive Antibodies (PRA) analysis is important not only in virtual cross-match of donors and recipients but also in follow-up of recipients immune response after transplantation. Although bead based tests give faster and more reliable, it may have false positive and negative results. We investigated HLA groups of patients with false negative results and the frequencies of anti-HLA antibodies in all three false negative situations. Materials and Methods: PRA results of all patients were divided into 3 groups according to negative controls and samples results. First one is negative controls were false negative and samples were false negative (1st Situation); second one is negative controls were false negative but samples were true negative (2nd Situation); third one is negative controls were true negative but samples were false negative (3rd Situation). All serum samples were tested by bead based Luminex assay. Results: While anti-HLA-A68, A24, A32 were the most frequent antibodies for the first situation, anti-HLA-A03,24,32 were the most frequent three antibodies for the second situation. In case of anti-HLA-B antibodies; anti-HLA-B38, B44, B48 were detected for the first situation, and anti-HLA-B44, B58, B49 were detected for the second situation. In case of class II antibodies; we detected anti-HLA-DRB110, DRB115 and DRB151 antibodies as the most frequent three antibodies at 1st situation. Frequencies of anti-HLA antibodies of 120 patients with false negative results were determined in serum samples. In case of 3rd situation, while anti-A23, A68, A24; anti-B06, B04, B39 and anti-Cw07 were the most frequent anti-HLA Class I antibodies, anti-HLA DQ07, DQ05, DQ04 and anti-HLA-DRB152, DRB113, DRB153 were the most frequent HLA-Class II antibodies detected in serum samples. Conclusion: Samples with false negative PRA results should be repeated and these samples should be recorded in the laboratory for internal control system.

Background/aims Lipoxin A4 (LXA4), an anti-inflammatory lipid mediator, regulates leukocyte cellular activity and activates gene transcription. The therapeutic effect of LXA4 on liver fibrosis and its mechanism on the immune system are largely unknown. Because the regenerative capacity of hepatocytes in acute and chronic liver failure models of mouse increases by silencing MKK4, we aimed to investigate the effect of parenteral administration of LXA4 on the genes responsible for regeneration of liver, namely MKK4, MKK7, and ATF2, and visualize the therapeutic effects in an experimental model. Materials and methods Fibrosis was induced in mice by administration of thioacetamide (TAA). LXA4 was administered during the last two weeks of fibrosis induction. The fibrosis level was measured by Knodell scoring. The liver function was measured by analyzing serum ALT, AST, and AP levels. Expression levels of genes responsible for liver fibrosis (TGF-α) and cell regeneration (MKK4, MKK7, and ATF2) have been measured by RT-PCR analysis. Inflammatory and anti-inflammatory cytokine levels were measured in serum samples and liver homogenates by Enzyme Linked Immunosorbent Assay (ELISA). Ultrathin sections were examined using a transmission electron microscope and analyzed. Results We observed significant healing in liver of the LXA4-treated group, histologically. This finding was in parallel with reduction of serum ALT, AST, but not AP levels. TGF-α and MKK4 expressions were significantly reduced in the LXA4-treated group. Administration of LXA4 caused significant elevation of IL-10 in systemic circulation; however, that elevation was not detected in liver homogenates. Nevertheless, significant reductions in TNF-α and IL-17 have been observed. Conclusion The anti-inflammatory effect of LXA4 maintains the regenerative capacity of liver during fibrosis in an experimental liver fibrosis model. LXA4 may be therapeutically beneficial in liver fibrosis.

INTRODUCTION[|]Brucellosis is a zoonotic disease caused by Brucella in domestic and wild animals. It also causes systemic diseases with the involvement of different parts of the human body. An efficient innate immune response is crucial to cure brucellosis with optimum antibiotic treatment. The inflammasomes are innate immune system receptors and sensors that regulate the activation of cysteine-dependent aspartate specific protease-1 (caspase-1) and caspase-1-induced cell death process known as pyroptosis. The aim of the present study was to investigate the expression levels of CASPASE-1 and associated inflammasomes AIM2, NLRP3, and NLRC4 to analyze their relationship with the inflammatory cytokine interleukin (IL)-1β, IL-18, and interferon-gamma (IFN-γ) in peripheral blood samples of patients with acute brucellosis with healthy controls.[¤]METHODS[|]Peripheral blood samples were obtained from 20 healthy volunteers and 20 patients with acute brucellosis. RNA and serum samples were isolated to examine the expression levels of AIM2, NLRP3, NLRC4, and CASPASE-1 by real-time polymerase chain reaction, and IL-1β, IL-18, and IFN-γ were measured by enzyme-linked immunosorbent assay.[¤]RESULTS[|]In the acute brucellosis group, AIM2 and NLRC4 expressions were significantly higher than in healthy volunteers. A significant increase on caspase-1 expression in patients with acute brucellosis was not observed. Serum IL-18 and IFN-γ levels were significantly higher in patients with acute brucellosis than in healthy controls.[¤]DISCUSSION AND CONCLUSION[|]Caspase-1-related inflammasomes are sufficiently activated to induce the secretion of cytokines, such as IFN-γ and IL-18, to induce cellular immune response. Caspase-1 activation level should be investigated at different periods of disease in a group with high number of patients to understand the role of pyroptosis and caspase-1 in brucellosis.[¤]

Amaç: Bu çalışmada klinik pratikte sık karşılaşılan, intramuskuler enjeksiyon sonrası siyatik siniri hasarını ratlarda oluşturulan deneysel periferik sinir hasarı modelinde değerlendirmeyi amaçladık.Gereç ve Yöntem: 78 adet erkek Wistar cinsi Albino rat, 5 ana gruba ayrıldı. Grup 1 (kontrol), grup 2 (sham), grup 3 (benzatil penisilin g), grup 4 (diklofenak sodyum) ve grup 5 (deksametazon) olarak gruplar tanzim edildi. Kontrol grubu haricindeki tüm grupların siyatik siniri eksplore edilerek epinöral, endonöral ve intrafasiküler mesafelere farmakolojik ajanlar tatbik edildi. Denekler fonksiyonel, elektrofizyolojik ve histopatolojik açılardan değerlendirildi.Bulgular: Her üç değerlendirme kriterine göre en belirgin ve istatistiki olarak anlamlı yaralanma benzatil penisilin G ve diklofenak sodyum gruplarında görülürken endonöral ve fasikül içi enjeksiyonların epinöral enjeksiyonlara nazaran daha belirgin hasar bıraktığı gözlendi. Sonuç: Bu çalışma ile periferik sinir trasesinde yapılacak herhangi bir ilaç enjeksiyonu fonksiyonel ve elektrofizyolojik kayıp ve/veya histolojik olarak periferik sinir mimarisinde bozulma etkileri olabileceğini gözlemlendi.Anahtar Kelimeler: Enjeksiyon nöropatisi, siyatik sinir, varyasyon, elektronöro monitörizasyon. Ojective: In this study we purposed to evaluate the sciatic nevre injury due to intramusculer injection which is frequently seen in medical practice on a rat experimental peripheral nevre injury model.Material and Method: 78 male Wistar albino rats are diveded into 5 major groups. We set the groups as group 1 (control), group 2 (sham), group 3 (benzatyl penicilline G), group 4 (diclofenac sodium) and group 5 (dexametasone). Pharmacological agents applied to all sciatic nerves of rats after exploration in epineural, endoneural and intrafasicular compartments except the control group. The subjects and their sciatic nerves evaluated with funcional, electrophysiological and histopathological results.Results: The injury which is evident and statistically significant is seen in benzatyl peniclline g and diclofenac sodium groups. On the other hand we have reached the result of the endoneural and intrafasicular injection may cause more harm than epineural injections.Conclusion: We observed that any medicine injection which can be applied on epineural, endoneural or intrafasicular compartments of sciatic nerve may cause functional and elctrophysiological loss with or without detoriation in peripheral nerve architecture.Key Words: injection neuropathy, sciatic nerve, variation, electroneuro monitor 81

The aim of this study is to determine the effect of hysteroscopic polypectomy on the mRNA expression levels of the endometrial receptivity markers, namely, homeobox A10 (HOXA10), homeobox A11 (HOXA11) and leukemia inhibitory factor (LIF). Twenty-five reproductive-aged women with endometrial polyps underwent hysteroscopy. Samples were taken at the mid-secretory phase using hysteroscopic polypectomy and 4 months after polypectomy, and the change in mRNA expression levels of normalized HOXA10, HOXA11 and LIF genes were determined using Reverse Transcription Quantitative Real Time-Polymerase Chain Reaction (RT-qPCR). The results show that mRNA levels of HOXA10 and HOXA11 taken prior to surgery and 4 months after the complete hysteroscopic removal of polyps were not significantly different (P=0.79 and P=0.14, respectively). Moreover, a marked difference could not be obtained between preoperative and postoperative endometrial LIF mRNA expression levels (P=0.86). As a conclusion, these results indicate that mRNA levels of HOXA10, HOXA11 and LIF genes, three of molecular markers of endometrial receptivity, are not affected by hysteroscopic polypectomy.

Bu tezde; gentamisin ile deneysel böbrek nefrotoksisitesi oluşturulmuş sıçanların böbrek dokusunda vasküler endotelyal büyüme faktör (VEGF-A) geni ifadesi ve kafeik asit fenetil esterin (CAPE) nefrotoksisitenin önlenmesindeki rolünün araştırılması amacıyla 32 adet Wistar cinsi dişi sıçan kullanıldı. Hayvanlar her grupta 8'er adet sıçan olmak üzere 4 gruba ayrıldı; Kontrol grubu (K; %10'luk dimetil sülfoksit (DMSO) intraperitonal yoldan verildi), Gentamisin grubu (G; 8 gün boyunca intraperitonal yolla 100 mg/kg/gün vücut ağırlığı dozunda gentamisin verildi), CAPE grubu (C; 30 mg/kg/gün vücut ağırlığı dozunda CAPE intraperitonal yolla 10 gün boyunca verildi), CAPE+Gentamisin grubu (C+G; 30 mg/kg/gün vücut ağırlığı dozunda CAPE ve 100 mg/kg/gün vücut ağırlığı dozunda gentamisin intaperitonal olarak beraber uygulandı). Deney sonunda gruplardan alınan böbrek dokularından VEGF-A gen ifadesi ve histopatalojik analizlerin yanısıra, serumdan BUN ve kreatinin analizleri yapıldı. Kontrol grubuna göre gentamisin uygulamasının böbrek VEGF-A gen ifadesini düşürdüğü (p0,05). Histopatolojik olarak kontrol grubuyla karşılaştırıldığında gentamisin uygulamasının böbrek dokusunda ciddi hasarlanmalara yol açtığı, CAPE uygulamasının ise bu hasarları kısmen iyileştirdiği tespit edildi. Kontrol grubuyla karşılaştırıldığında gentamisin uygulanan hayvanların serum kreatinin ve BUN değerlerinin anlamlı derece yükseldiği (p0,05). Sonuç olarak gentamisin uygulamasının böbrek VEGF-A gen ifadesini ciddi bir şekilde azalttığı, gentamisin kaynaklı böbrek hasarında VEGF-A'nın bozulan ifadesinin önemli bir rol oynayabileceği, CAPE uygulamasının ise gentamisin kaynaklı toksisitenin önlenmesinde önemli bir etkisi olmadığı kanaatine varıldı. In this thesis, 32 Wistar female rats were used to investigate vascular endothelial growth factor (VEGF-A) gene expression and the protective role of caffeic acid phenethyl ester (CAPE) against gentamicin induced experimental renal nephrotoxicity model of rat kidney tissue. Animals in each group of eight rats were divided into 4 groups including; Control group (N; 10% dimethyl sulfoxide (DMSO) intraperitoneally given), Gentamicin group (G; 8 days via i.p. route, 100 mg/kg/day body weight gentamicin was intraperitoneally given), CAPE (C; 30 mg/kg/day body weight CAPE was given for 10 days), CAPE + gentamicin group (C + G; 30 mg/kg/day body weight CAPE and 100 mg/kg/day body weight gentamicin intaperitonal were applied together). At the end of the experiment, histopathology, VEGF-A gene expression, as well as serum BUN and creatinine levels were analyzed from the kidney tissue of groups. Gentamicin administration decreased the kidney VEGF-A gene expression compared to control group (p 0,05). Histopathologically, gentamicin application caused serious damage in the kidney tissue compared with the control group and the CAPE application was found to improve the damage partially. Gentamicin administiration significantly increased serum creatinine and BUN values compared with controls (p 0.05). As a result, gentamicin application significantly reduces kidney VEGF-A gene expression and altered VEGF-A gene expression could play an important role in gentamicin-induced renal injury. It is concluded that CAPE administration did not have any significant effect in preventing gentamicin-induced toxicity. 82