Dexamethasone and concentrated growth factors on peripheral nerve injury: A clinic-relevant animal study.

BACKGROUND: Mandibular nerve injury is a common clinical condition that affects clinicians' management and patients' quality of life. In the literature, there are various effective treatments available. The primary purpose of this study was to determine and compare the effects of dexamethasone and concentrated growth factor (CGF) on regeneration in patients with nerve trauma that mimics clinical situations. METHODS: In this study, 36 rats were divided into 3 groups: the control, dexamethasone and CGF groups. The inferior alveolar nerve was traumatized through the extraction socket after mandibular molar tooth extraction in each group. RESULTS: The data showed a decrease in the control (4.5-4), dexamethasone (3-2), and CGF (4-3) groups according to the histological injury severity score (HISS) results. Compared with those in the other groups, the number of degenerative axons and edematous areas observed via histological examination were significantly lower in the CGF groups. Similarly, compared with those in the control group, the nNOS and Neurofilament-H positivity in the dexamethasone group on the 30th day (2,2 to 1,1 respectively) was significantly lower. The positivity of all the primary antibodies in the 3rd and 30th day CGF groups was significant compared than that in the dexamethasone 30th day group. CONCLUSION: According to the results of the analysis of the immunohistopathological and HISS data, the CGF groups exhibited greater regeneration than did the dexamethasone groups.

The effects of dexmedetomidine on trauma-induced secondary injury in rat brain.

BACKGROUND: The objective of this study was to investigate the effect of dexmedetomidine (Dex), a sedative drug with little or no depressant effect on respiratory centers, on secondary injury in rat brain tissue by means of the Na+/K+ ATPase enzyme, which maintains the cell membrane ion gradient; malondialdehyde, an indicator of membrane lipid peroxidation; glutathione, an indicator of antioxidant capacity; and histopathological analyses. METHODS: Eighteen rats were randomized into three groups: the trauma group received anesthesia, followed by head trauma with a Mild Traumatic Brain Injury Apparatus; the Trauma+Dex group received an additional treatment of 100 µg/kg intraperitoneal dexmedetomidine daily for three days; the Control group received anesthesia only. RESULTS: The highest MDA levels compared to the Control group were found in the Trauma group. Mean levels in the Trauma+Dex group were lower, albeit still significantly high compared to the Control group. Glutathione levels were similar in all groups. Na/K-ATPase levels were significantly lower in the Trauma group compared to both the Control group and the Trauma+Dex group. Histopathologic findings of tissue degeneration including edema, vascular congestion and neuronal injury, and cleaved caspase-3 levels were lower in the Trauma+Dex group compared with the Trauma group. CONCLUSIONS: Dexmedetomidine administered during the early stage of traumatic brain injury may inhibit caspase-3 cleavageHowever, the mechanism does not seem to be related to the improvement of MDA or GSH levels.

The potential antioxidant effect of N-acetylcysteine on X-ray ionizing radiation-induced pancreas islet cell toxicity.

PURPOSE: Previous research has highlighted the impact of X-ray irradiation-induced organ damage, on cancer patients after radiation therapy. The ionizing radiation-induced oxidative stress causes injury to the pancreatic islet cells of Langerhans. We used histopathological, immunohistochemical, and biochemical analyses to examine α- and ß-cells in the islets of Langerhans in rats undergoing whole-body x-ray ionizing radiation, a group of which was treated with NAC. MATERIAL AND METHODS: Twenty-four male rats were randomly divided into 3 groups, one control, and two experimental groups. Group I (Control) was administered only saline solution (0.09% NaCl) by oral gavage for 7 days. Group II (IR) was administrated whole body single dose 6 Gray ionizing radiation (IR) and saline solution (0.09% NaCl) by oral gavage for 7 days. Group III (IR + NAC) was administered 300 mg/kg NAC (N-acetylcysteine) by oral gavage for 7 days, 5 days before, and 2 days after 6 Gray IR application. RESULTS: In the X-ray irradiation group, we observed diffuse necrotic endocrine cells in the islets of Langerhans. In addition, we found that Caspase-3, malondialdehyde (MDA) levels increased, and insulin, glucagon, and glutathione (GSH) levels decreased in the IR group compared to the control group. In contrast, we observed a decrease in Caspase-3, and MDA levels in necrotic endocrine cells, and an increase in insulin, glucagon, and GSH levels in the IR + NAC group compared to the IR group. CONCLUSION: This study provides evidence for the beneficial effects of N-acetyl cysteine on islets of Langerhans cells with X-ray ionizing-radiation-induced damage in a rat model.

Resveratrol Attenuates Degeneration and Apoptosis of Cardiomyocytes Induced by Aortic Clamping.

INTRODUCTION: Objective: To investigate the potential beneficial effects of resveratrol (RVT) against ischemia-reperfusion injury of myocardial tissue during surgical treatment of ruptured abdominal aortic aneurysm. METHODS: Four groups were established - control, ischemia/reperfusion (I/R), sham (I/R+solvent/dimethyl sulfoxide [DMSO]), and I/R+RVT. Ruptured abdominal aortic aneurysm model was used as the experimental protocol. RESULTS: In the I/R and I/R+DMSO groups, malondialdehyde (MDA) levels in myocardial tissue were found to be significantly increased compared to the control group. The MDA level in myocardial tissue was significantly decreased in the I/ R+RVT group compared to the I/R group. In I/R and I/R+DMSO groups, glutathione peroxidase (GSH) levels in myocardial tissue were found to be significantly decreased compared to the control group. The GSH level in the myocardial tissue was significantly increased in the I/R+RVT group compared to the I/R group. In the light microscope, isotropic and anisotropic band disorganized atypical cardiomyocytes in the I/R group and degenerative cardiomyocytes and edematous areas in the I/R+DMSO group were observed. Degenerative cardiomyocytes and edematous areas were decreased in the I/R+RVT group. When heart tissue sections incubated with cleaved caspase-3 primary antibodies were examined under the light microscope, apoptotic cardiomyocytes were present in I/R and I/R+DMSO groups. A decrease in the number of apoptotic cardiomyocytes was observed in the I/R+RVT group. CONCLUSION: The findings of the present study indicate that RVT exhibits protective effects against ischemia-reperfusion injury occurring in the myocardium as a distant organ as a result of abdominal aorta clamping.

The Effects of White Tea (Camellia Sinensis) and Infliximab Against Cisplatin- Induced Testicular Damage via Oxidative Stress and Apoptosis / Efectos del Té Blanco (Camellia Sinensis) e Infliximab Contra el Daño Testicular Inducido por Cisplatino a Través del Estrés Oxidativo y la Apoptosis

SUMMARY: Cisplatin (Cis) is an important chemotherapeutic agent used in cancer treatment. Males exposed to Cis were reported to exhibit testicular toxicity. Cis-induced testicular toxicity is mediated by oxidative stress, inflammation, testosterone inhibition and apoptosis. Accordingly, this study was conducted to evaluate the potential protective roles of infliximab (IFX), which is an anti- TNF-a agent, and of white tea (Camellia sinensis), which is known to possess antioxidant, anti-apoptotic, and anti-inflammatory effects, against Cis-induced testicular toxicity in rats. Rats were randomly assigned into five groups as follows: control group, Cisplatin (7 mg/kg) treatment group, Cisplatin (7 mg/kg) + infliximab (7 mg/kg) treatment group, cisplatin + white tea (WT) treatment group, and Cisplatin+ WT+IFX combined treatment group. In the present study, Cis exposure reduced the sperm count. It also increased testicular oxidative stress as well as the levels of inflammatory and apoptotic markers. Histopathological assays supported the biochemical findings. Treatment with IFX and/or WT restored testicular histology, preserved spermatogenesis, suppressed oxidative stress and apoptosis, and significantly ameliorated Cis-induced damage. It was concluded that white tea and infliximab could potentially serve as therapeutic options for the protection of testicular tissue against the harmful effects of Cis.

El cisplatino (Cis) es un importante agente quimioterapéutico utilizado en el tratamiento del cáncer. Se informó que los hombres expuestos a Cis exhibieron toxicidad testicular. La toxicidad testicular inducida por Cis está mediada por el estrés oxidativo, la inflamación, la inhibición de la testosterona y la apoptosis. En consecuencia, este estudio se realizó para evaluar las posibles funciones protectoras de infliximab (IFX), un agente anti-TNF-α, y del té blanco (Camellia sinensis), conocido por sus propiedades antioxidantes, antiapoptóticas y anti-TNF-α -efectos inflamatorios, contra la toxicidad testicular inducida por Cis en ratas. Cinco grupos de ratas se asignaron al azar de la siguiente manera: grupo control, grupo de tratamiento con cisplatino (7 mg/ kg), grupo de tratamiento con cisplatino (7 mg/kg) + infliximab (7 mg/kg), grupo de tratamiento con cisplatino + té blanco (WT), y grupo de tratamiento combinado Cisplatino+ WT+IFX. En el presente estudio, la exposición a Cis redujo el conteo de espermatozoides. También aumentó el estrés oxidativo testicular, así como los niveles de marcadores inflamatorios y apoptóticos. Los ensayos histopatológicos respaldaron los hallazgos bioquímicos. El tratamiento con IFX y/o WT restauró la histología testicular, preservó la espermatogénesis, suprimió el estrés oxidativo y la apoptosis, y mejoró significativamente el daño inducido por Cis. Se concluyó que el té blanco y el infliximab podrían potencialmente servir como opciones terapéuticas para la protección del tejido testicular contra los efectos nocivos de Cis.

The protective effects of ginseng on x-irradiation-induced intestinal damage in rats.

Although radiotherapy is widely employed in the treatment of various malignancies in oncology patients, its use is limited by the toxic effects it causes in surrounding tissues, including the gastrointestinal system. Korean Red Ginseng (KRG) is a traditional drug reported to possess antioxidant and restorative properties in various studies. The purpose of the present study was to investigate the protective effects of KRG against radiation-associated small intestinal damage. Twenty-four male Sprague Dawley rats were randomly assigned into three groups. No procedure was performed on Group 1 (control) during the experiment, while Group 2 (x-irradiation) was exposed to radiation only. Group 3 (x-irradiation + ginseng) received ginseng via the intraperitoneal route for a week prior to x-irradiation. The rats were killed 24 h after radiation. Small intestinal tissues were evaluated using histochemical and biochemical methods. An increase in malondialdehyde (MDA) levels and a decrease in glutathione (GSH) were observed in the x-irradiation group compared to the control group. KRG caused a decrease in MDA and caspase-3 activity and an increase in GSH. Our findings show that it can prevent damage and apoptotic cell death caused by x-irradiation in intestinal tissue and can therefore play a protective role against intestinal injury in patients receiving radiotherapy.

Protective Effect of Vaccinium myrtillus Extract on X-ray Irradiation-Induced Retinal Toxicity via eNOS and 8-OHdGexpression.

Every year, hundreds of thousands of cancer patients receive radiotherapy treatment. Oxidative stress is observed in healthy tissues due to irradiation exposure. The present study is the first to address the effects of Vaccinium myrtillus (whortleberry, WB) against the effects of x-ray irradiation on retinal tissue. Twenty-four Sprague-Dawley rats were randomly allocated into 4 groups: (1) control group: rats without any treatment, (2) x-ray irradiation group: 8 Gray (Gy) RT for 2 days, (3) 100 mg WB extract + x-ray irradiation group: 8 Gy irradiation for 2 days and followed by intraperitoneal (IP) WB extract (100 mg/kg) supplementation for 10 days, (4) 200 mg WB extract + x-ray irradiation group: 8 Gy irradiation for 2 days and followed by intraperitoneal (IP) WB extract (200 mg/kg) supplementation for 10 days. Eyes were enucleated on the 10th day after RT for histopathological, immunohistochemical (8-hydroxy deoxyguanosine (8-OHdG), endothelial nitric oxide synthase (eNOS), and biochemical analyses (glutathione peroxidase (GSH), and malondialdehyde (MDA). The GSH levels significantly decreased and MDA levels and 8-OHdG staining increased after x-ray irradiation compared to the control group. Combined x-ray irradiation +WB treatment significantly increased GSH levels and significantly decreased MDA production and 8-OHdG staining. However, eNOS staining was not affected in any of the groups. Besides, x-ray irradiation significantly increased cell losses and edematous areas. The WB significantly reversed the cellular damage in ganglion cells, inner nuclear, and outer nuclear layers in quantitative analyses. The x-ray irradiation caused significant retinal impairment, and additional WB therapy provided protective effects against radiation-induced retinopathy. These results may suggest WB extract as an adjuvant therapy to reverse retinal impairments after x-ray irradiation.

Agomelatine on cisplatin-induced nephrotoxicity via oxidative stress and apoptosis.

Drug-induced nephrotoxicity is the greatest deterrent to the use of cisplatin, which is a frequently used chemotherapeutic with proven effectiveness in cancer therapy. Agomelatine, which is used in the treatment of sleep disorders and depression, has gained attention in recent years with its antioxidative and anti-inflammatory effects. In this study, the effects of the synthetic melatonin agonist agomelatine on nephrotoxicity were investigated in a rat model of cisplatin-induced nephrotoxicity using biochemical, histological, and immunohistochemical methods. Thirty-two male rats were divided into 4 groups: 1. control group, 2. agomelatine group, 3. cisplatin group, 4. cisplatin + agomelatine group. In the cisplatin group, there were widespread atypical glomerular structures and vacuolization in tubular epithelial cells, necrotic tubules, deterioration of brush border structure in proximal tubules, and fibrotic areas characterized by diffuse polymorphonuclear leukocyte (PNL) and extensive collagen deposition in the interstitial spaces. However, in the cisplatin + agomelatine group, we observed a reduction in glomeruli of atypical structure and necrotic tubules, in PNL infiltration in interstitial spaces, and fibrotic areas compared to the cisplatin group. The cisplatin + agomelatine group showed lower malondialdehyde (MDA) serum creatinine, serum urea levels, and higher glutathione (GSH) levels compared to the cisplatin group. Immunohistochemical analyses revealed that the elevated NF-kß/p65, 8-OHdG, and cleaved caspase-3 positivity in the cisplatin group had significantly decreased in the cisplatin + agomelatine group. In conclusion, agomelatine showed a nephroprotective effect against cisplatin-induced nephrotoxicity.

The Effects of Dexmedetomidine on Abdominal Aortic Occlusion-Induced Ovarian Injury via Oxidative Stress and Apoptosis.

Ischemia/reperfusion (I/R) induced ovarian damage is caused by various diseases such as ovarian torsion, ovarian transplantation, cardiovascular surgery, sepsis, or intra-abdominal surgery. I/R-related oxidative damage can impair ovarian functions, from oocyte maturation to fertilization. This study investigated the effects of dexmedetomidine (DEX), which has been shown to exhibit antiapoptotic, anti-inflammatory, and antioxidant effects, on ovarian I/R injury. We designed four study groups: group 1 (n = 6): control group; group 2 (n = 6): only DEX group; group 3 (n = 6): I/R group; group 4 (n = 6): I/R + DEX group. Then, ovarian samples were taken and examined histologically and immunohistochemically, and tissue malondialdehyde (MDA) and glutathione (GSH) levels were measured. In the I/R group MDA levels, caspase-3, NF-κB/p65, 8-OHdG positivity, and follicular degeneration, edema, and inflammation were increased compared to the control group (p = 0.000). In addition, GSH levels were significantly decreased in the I/R group compared to the control group (p = 0.000). On the other hand, in the I/R + DEX treatment group MDA levels, caspase-3, NF-κB/p65, 8-OHdG positivity, follicular degeneration, edema, and inflammation findings were decreased than in the I/R group (p = 0.000, p = 0.005, p = 0.005, p = 0.001, p = 0.005, respectively). However, GSH levels increased significantly in the I/R + DEX treatment group compared to the I/R group (p = 0.000). DEX protects against ovarian I/R injury through antioxidation and by suppressing inflammation and apoptosis.

Agomelatine attenuates cisplatin-induced cognitive impairment via modulation of BDNF/TrkB signaling in rat hippocampus.

Cisplatin is a drug used effectively in the treatment of malignant tumors. However, cisplatin has many side effects, including cognitive impairment. Agomelatine, a synthetic melatonin analogue, is an important antidepressant. Increasing evidence has shown that agomelatine may be a potential neuroprotective agent. The aim of this study was to investigate the effect of agomelatine on learning and memory functions in cisplatin-induced cognitive impairment in a rat model. Male rats were administered agomelatine and cisplatin for 4 weeks. Neurobehavioral tests were performed at the end of the 4th week. After behavioral tests, rats were euthanized and BDNF, TNF, IL-1ß, MDA and GSH levels were measured in hippocampal homegenates by ELISA. In addition, nNOS and TrkB receptor activity were measured immunohistochemically. The results showed that agomelatine significantly improved cognitive functions in spatial memory tests in rats with cisplatin-induced cognitive impairment. In addition, agomelatine treatment positively affected the discrimination index (DI). On the other hand, agomelatine treatment elevated cisplatin-suppressed hippocampal BDNF levels. Agomelatine treatment reduced cisplatin-induced neuroinflammation by suppressing TNF and IL-1ß levels. Similarly, agomelatine reduced oxidative stress in the hippocampus. Histological findings showed that agomelatine treatment reduced pyramidal neuron damage in hippocampal DG, CA1 and CA3. Cisplatin increased nNOS and TrkB positivity in DG, CA1 and CA3 neurons compared to control. In contrast, agomelatine treatment decreased both nNOS and TrkB positive scores. These findings indicate that agomelatine reduces cisplatin-related cognitive impairment by exerting anti-inflammatory action and possibly by the modulation of the BDNF/TrkB/nNOS pathways in the hippocampus.

Neuroprotective effects of Vaccinium myrtillus on damage-related brain injury.

Traumatic brain injury may trigger the secondary brain injury, which has the potential to be reversible and thus preventable. Anthocyanins are phylotherapeutic plants, which are reported to exhibit anti-inflammatory properties. This study aimed to evaluate the therapeutic efficiency of an anthocyanin, namely Vaccinium myrtillus, to alleviate secondary brain injury and identify possible mechanism of actions. It is hypothesized that lipid peroxidation and Na+ -K+ -ATPase activity may be involved in neuronal ischemia. Thus, brain tissue Malondialdehyde content, Na+ -K+ -ATPase content, and cleaved caspase-3 content was investigated following moderate head trauma in a rat model. Twenty-four Sprague-Dawley male rats were allocated into four groups: Control, Trauma, Solvent-Control, and Treatment. Trauma and Solvent-Control groups showed more prominent brain edema, neuronal ischemia, vascular congestion, increase in brain tissue Malondialdehyde and cleaved caspase-3 levels, and decreased Na+-K+-ATPase activity compared to the Control group. Although the Treatment group had comparable histological signs to the Trauma and Solvent-Control groups, Malondialdehyde level and Na+-K+-ATPase activity was similar to Control group, and cleaved caspase-3 levels were lower compared to Trauma and Solvent-Control groups. We conclude that anthocyanin extracts may alleviate secondary brain injury via anti-oxidative and anti-apoptotic mechanisms.

Histopathological evaluation of the effects of dexmedetomidine against pituitary damage induced by X-ray irradiation.

Background: The present study, aimed to investigate the potential negative effects of x-ray radiation and the effects of the α2-adrenergic receptor agonist dexmedetomidine on the pituitary gland.Methods: Twenty-four Sprague-Dawley rats were divided into three groups: Rats in Group 1 (control group). Group 2 (X-ray irradiation) and group 3 (X-ray irradiation + Dexmedetomidine) were given a total of 10 Gy external beam total body irradiation. Group 3 was given a single intraperitoneal dose of 200 µg/kg dexmedetomidine 30 minutes before RT.Results: In sections obtained from the x-ray irradiation group, we observed many necrotic in adenohypophysis and neurohypophysis. In addition, there were extensive oedematous areas and vascular congestions due to the necrotic cells in both the adenohypophysis and neurohypophysis. In contrast, we observed a reduction in necrotic chromophobic and chromophilic cells in adenohypophyseal tissue and a reduction in necrotic pituicytes in neurohypophyseal tissue in the dexmedetomidine treatment group. In addition, we determined lower caspase-3 and TUNEL expression in the dexmedetomidine treatment group compared with the x-ray irradiation group. Dexmedetomidine reduced x-ray radiation-induced pituitary damage by preventing apoptosis.Conclusions: The present study demonstrated the use of dexmedetomidine in situations related to radiation toxicity and offers the potential for a comprehensive study.

Inhibition of methotrexate induced toxicity in the adult rat spleen by adalimumab.

Methotrexate (MTX) has been in use for the treatment of rheumatoid arthritis (RA), psoriasis, and cancer since 1948. Its toxic side effects on tissues and organs have been well documented but splenotoxicity has not been addressed. This study set out to investigate this issue by examining the effectiveness of anti-TNFα agents against MTX-induced toxicity in T lymphocytes and macrophages via the regulation of CD3, CD68, and CD200R. Twenty-four Sprague Dawley rats were allocated to three groups: control (received saline solution only), MTX (20 mg/kg of single-dose of MTX), and Ada + MTX (single dose of 10 mg/kg Adalimumab before MTX administration). The spleens were removed 5 days after MTX administration. The number of CD3+/mm3cells for the control, MTX and Ada + MTX groups were, respectively, 2.69 ± 0.86, 20.51 ± 2.7, (p = 0.000) and 11.07 ± 2.01 (p = 0.000). The number of CD68+ macrophages/mm3 in the control, MTX and Ada + MTX groups were, respectively, 8.62 ± 1.08, 38.19 ± 1.37 (p = 0.000), and 16.87 ± 12.57 (p = 0.000). The number of macrophages that were CD200R+/mm3 in the control, MTX, and Ada + MTX groups were 3.33 ± 1.66, 25.77 ± 2.37 (p = 0.000), and 8.68 ± 2.66 (p = 0.000), respectively. We also observed that Ada reduced the numerical densities of these cells following MTX administration (p < 0.05). Ada may, therefore, be a promising candidate for the prevention of the deleterious effects on T lymphocytes and macrophages of MTX-induced toxicity.

Resveratrol Attenuates Degeneration and Apoptosis of Cardiomyocytes Induced by Aortic Clamping

ABSTRACT Introduction: Objective: To investigate the potential beneficial effects of resveratrol (RVT) against ischemia-reperfusion injury of myocardial tissue during surgical treatment of ruptured abdominal aortic aneurysm. Methods: Four groups were established — control, ischemia/reperfusion (I/R), sham (I/R+solvent/dimethyl sulfoxide [DMSO]), and I/R+RVT. Ruptured abdominal aortic aneurysm model was used as the experimental protocol. Results: In the I/R and I/R+DMSO groups, malondialdehyde (MDA) levels in myocardial tissue were found to be significantly increased compared to the control group. The MDA level in myocardial tissue was significantly decreased in the I/ R+RVT group compared to the I/R group. In I/R and I/R+DMSO groups, glutathione peroxidase (GSH) levels in myocardial tissue were found to be significantly decreased compared to the control group. The GSH level in the myocardial tissue was significantly increased in the I/R+RVT group compared to the I/R group. In the light microscope, isotropic and anisotropic band disorganized atypical cardiomyocytes in the I/R group and degenerative cardiomyocytes and edematous areas in the I/R+DMSO group were observed. Degenerative cardiomyocytes and edematous areas were decreased in the I/R+RVT group. When heart tissue sections incubated with cleaved caspase-3 primary antibodies were examined under the light microscope, apoptotic cardiomyocytes were present in I/R and I/R+DMSO groups. A decrease in the number of apoptotic cardiomyocytes was observed in the I/R+RVT group. Conclusion: The findings of the present study indicate that RVT exhibits protective effects against ischemia-reperfusion injury occurring in the myocardium as a distant organ as a result of abdominal aorta clamping.

Celastrol restricts experimental periodontitis related alveolar bone loss by suppressing inflammatory cytokine response.

Introduction: Periodontitis is a common chronic inflammatory disease characterized by the destruction of the supporting structures of the teeth. The host defense mechanisms are responsible for inflamatuar and destructive reactions in periodontitis. Celastrol is one of the most promising components of the plant in Eastern and Southern China that has a long history of use in traditional medicine for the treatment of inflammatory conditions. Aim: The aim of this animal study was to inspect the preventive or restrictive effects of celastrol on periodontitis-related inflammatory host response and alveolar bone loss. Methods: 24 male Sprague Dawley rats were randomly assigned into 3 groups: control, experimental periodontitis (Ep), and experimental periodontitis-celastrol (Ep-Cel). Periodontitis was induced by placing ligatures sub-paramarginally around the mandibular first molars of the rats in the Ep and Ep-Cel groups and maintaining the ligatures for 15 days. For 14 days following the ligature placement, celastrol administration (1 mg/kg BW day) for the Ep-Cel group and vehicle injection for the control and Ep groups was carried out. At the end of the experiment, mandibula and gingiva samples were obtained after the euthanasia. Alveolar bone loss was measured on serial histological slices; Tumor Necrosis Factor-α and Interleukin-1ß levels were measured on gingiva samples by ELISA. Results: Systemic celastrol administration significantly restricted the alveolar bone loss that was higher in rats with periodontitis. (p < 0.05) Tumor Necrosis Factor-α and Interleukin-1ß levels that were high in the gingiva of the rats with periodontitis were found significantly lower in rats administered celastrol. (p < 0.05). Conclusion: Celastrol restricted periodontitis-related alveolar bone loss by suppressing the inflammatory response.

The protective effects of red ginseng and amifostine against renal damage caused by ionizing radiation.

This study aimed to elucidate the effects of amifostine (ethyol) (AM), a synthetic radioprotector, and red ginseng (RG), a natural radioprotective agent, against the toxic effect of ionizing radiation (IR) on kidney tissues through changes in biochemical and histopathological parameters in addition to contributions to the use of amifostine and RG in clinical studies. Five groups were established: Group I (control, receiving only saline by gavage), Group II (IR only), and Group III (IR+AM, 200 mg/kg intraperitoneally (i.p.). Group IV (IR + RG, 200 mg/kg orally once a day for 4 weeks), and Group V (IR+RG+AM, 200 mg/kg orally once/day for 4 weeks before IR and 200 mg/kg AM administered (i.p.) 30 min before IR). All groups, except for the control group, were subject to 6-Gy whole-body IR in a single fraction. 24 h after irradiation, all animals were sacrificed under anesthesia. IR enhanced MDA, 8-OHdG, and caspase-3 expression while decreasing renal tissue GSH levels (p < .05). Significant numbers of necrotic tubules together with diffuse vacuolization in proximal and distal tubule epithelial cells were also observed. The examination also revealed substantial brush boundary loss in proximal tubules as well as relatively unusual glomerular structures. While GSH levels significantly increased in the AM, RG, and AM+RG groups, a decrease in KHDS, MDA, 8-OHdG, and caspase-3 expression was observed, compared to the group subject to IR only (p < .05). Therefore, reactive oxygen species-scavenging antioxidants may represent a promising treatment for avoiding kidney damage in patients receiving radiation.

Dexmedetomidine attenuates pneumocyte apoptosis and inflammation induced by aortic ischemia-reperfusion injury.

OBJECTIVE: Despite significant improvements in interventional vascular aneurysm repair procedures and intensive care patient management, there has been no significant decrease in mortality due to ruptured abdominal aortic aneurysm. Oxidative stress is known to play a key role in secondary organ damage due to infrarenal aortic clamping. The aim of this study was to examine the potential protective effect of the alpha-2 adrenergic receptor agonist dexmedetomidine (DMT) on aortic occlusion-induced lung injury. METHODS: Thirty Sprague Dawley rats were allocated into control, ischemia-reperfusion (IR), and IR+DMT groups randomly. Vascular clamps were attached to the abdominal aorta in the IR and IR+DMT groups. Two-hour reperfusion was established 1 h after ischemia. The IR+DMT group received a single intraperitoneal 100 µg dose of DMT 30 min before infrarenal abdominal aortic clamping. RESULTS: IR due to aortic occlusion led to apoptosis, widespread inflammation, alveolar septal wall thickening due to bleeding and vascular congestion were observed in both types I and II pneumocytes. Malondialdehyde levels increased while glutathione decreased. However, DMT was found to lower apoptotic pneumocytes, alveolar-septal thickness, hemorrhage, vascular congestion, and malondialdehyde levels, while glutathione levels in lung tissue increased. CONCLUSIONS: This study is the first to address the effects of DMT on the lung in a ruptured abdominal aortic aneurysm model. Our findings suggest that the alpha-2 adrenergic receptor agonist DMT reduces oxidative stress and apoptosis, thus protecting against aortic occlusion-induced pulmonary injury.

Effects of gadodiamide and gadoteric acid on lung tissue: A comparative study.

We set out to investigate the effects of gadodiamide and gadoteric acid, used for magnetic resonance imaging, on the lungs. In this study, 32 male Sprague Dawley rats were used. These were allocated into four groups; The first group (control) was untreated. The second group received isotonic saline on the first and fourth days of the week for 5 weeks. Following the same schedule, the third and fourth groups received a total of 2 mg/kg gadodiamide and gadoteric acid, respectively, in place of saline. The alveolar Wall thickness was evaluated. Gadodiamide and gadoteric acid significantly increased the numbers of collagen-3 and caspase-3 positive cells in the lung tissue (p < 0.05). In addition, these two substances increased the alveolar Wall thickness (p < 0.05). Furthermore, they increased the levels of malondialdehyde and glutathione (p < 0.05). This study demonstrates that both linear and macrocyclic contrast agents are toxic for the lungs in rats.

The cardioprotective effects of perindopril in a model of polymicrobial sepsis: The role of radical oxygen species and the inflammation pathway.

Mortality rates associated with myocardial dysfunction due to sepsis and septic shock are generally high across the world. The present study focused on the antioxidant and anti-inflammatory effects of perindopril (PER) for the purpose of preventing the adverse effects of sepsis on the myocardium and developing new alternatives in treatment. The control group received only saline solution via the oral route for 4 days. The second group underwent cecal ligation puncture (CLP), and the third underwent CLP and received PER (2 mg/kg). Rats in the third group received 2 mg/kg PER per oral (p.o.) from 4 days before induction of sepsis. Thiobarbituric acid reactive species (TBARS), total thiol (-SH), interleukin-1 beta (IL-1ß), IL-6, 8-hydroxy-2'-deoxyguanosine (8-OHdG), and nuclear factor kappa B (NF-κB/p65) levels increased in the CLP groups. In contrast, PER (2 mg/kg) decreased the levels of biochemical parameters other than total-SH and decreased 8-OHdG, NF-κB/p65 immunopositivity in rat heart tissues. The data from this study show that impairment of the oxidant/antioxidant balance and inflammatory cytokine levels in favor of inflammation in heart tissue under septic conditions results in severe tissue damage. PER administration before sepsis was shown to exhibit antioxidant and anti-inflammatory properties by reducing these effects. This in turn increased the importance of PER as new evidence of its protective effects in heart tissue.

Clinical and Histologic Evaluation of Partial Achilles Tendon Injury Repair with Amniotic Membrane in Rats.

BACKGROUND: Adhesions after tendinopathy in individuals who perform physical work and those physically active in middle age are a challenging problem for orthopedic surgeons. We evaluated the effects of human-derivated amniotic membrane on tendon healing, adhesions, angiogenesis, and the inflammatory process. METHODS: Thirty-five rats were divided evenly into five groups, and the left lower extremity was used in this study. No interventions were applied to the control group (group 5). In the other groups, Achilles tendons were partially cut to the midline. Then, primary repair (group 1), amniotic membrane treatment with no repair (group 2), primary repair and amniotic membrane treatment (group 3), or secondary healing with no repair (group 4) was performed. RESULTS: Use of amniotic membrane in tendon healing resulted in decreased adhesion formation and positive effects on collagen sequencing and anti-inflammatory effects. In addition, for the vascular endothelial growth factor evaluation there was no difference among the amniotic membrane repair groups, but there was an increase in vascular endothelial growth factor positivity compared with the control group. CONCLUSIONS: These data show that amniotic membrane treatment can alter biological behavior and induce surface-dependent angiogenesis and can have angiogenetic effects on ischemia and inflammation.