Spraque-Dawley Rats Research Articles

Effects of Pinealectomy and Melatonin Supplementation on Elements Metabolism in Rat Testicular Tissue

Objective: The aim of this study was to investigate how pinealectomy and melatonin application affect elements metabolism in rat testicular tissue. Methods: The study was carried out on 32 adult male Spraque-Dawley rats. Animals were divided into 4 equal groups. Group 1: Control, Group 2: Melatonin, Group 3: Pinealectomy, Group 4: Pinealectomy+Melatonin. Group 2 and 4 animals received daily 3mg/kg intraperitoneal (ip) melatonin supplementation for 4 weeks. The pineal glands of Group 3 and 4 animals were removed under general anesthesia. At the end of the applications, testicular tissue samples were taken from the animals sacrificed under general anesthesia. Elemental determinations (µg/gram/tissue) were performed in testicular tissue samples using the atomic emission method. Results: The highest cobalt, molybdenum, nickel, manganese, phosphorus, and sodium levels (p<0.001) and the lowest potassium levels in the testicular tissue were obtained in the pinealectomy group (group 3) (p<0.001). Magnesium and selenium values in testicular tissue were highest in the pinealectomy group (group 3) (p<0.001), and were higher in the pinealectomy+melatonin group (group 4) than ingroup 1 (control) and group 2 (melatonin) (p<0.001). Testicular zinc levels were highest in group 2, where melatonin was administered, and lowest in group 3, which was the pinealectomy group (p<0.001). Conclusion: The findings obtained as a result of the study show that pinealectomy significantly disrupts element metabolism in the testicular tissue of rats, and melatonin supplementation may have a regulatory effect on testicular elemental metabolism.

Endothelial dysfunction is dampened by early administration of fresh frozen plasma in a rodent burn shock model.

Endothelial dysfunction has been implicated in the pathogenesis of burn shock affecting patients with large thermal injury. In response to injury, glycocalyx components like Syndecan-1 (SDC-1) are shed into circulation and have been used as markers of endothelial damage. Previous work in our laboratory has shown that plasma inclusive resuscitation (PIR) with fresh frozen plasma (FFP) ameliorates endothelial damage. However, there remains a paucity of information regarding optimal timing and dosing of PIR as well as organ-specific endothelial responses to shock. We aimed to examine the impact of PIR on endothelial dysfunction using clinically translatable timing and dosing. Sprague-Dawley rats were used to create thermal burns. Rats were subjected to 40% total body surface area scald burns and were resuscitated with lactated Ringer's (LR) only, LR plus albumin, and LR plus early 1 mL boluses of FFP at 0, 2, 4, and 8 hours postinjury. A late group also received LR plus FFP starting at hour 10 postinjury. Syndecan-1 levels were quantified by enzyme-linked immunosorbent assay, and quantitative real-time polymerase chain reaction analysis characterized transcription of glycocalyx components and inflammatory cytokines in the lung and spleen. Evan's blue dye was used to quantify amount of vascular leakage. Lactated Ringer's plus early FFP reduced Evan's blue dye extravasation when compared with LR only groups, while late FFP did not. When comparing LR only versus LR plus early FFP, SDC-1 levels were reduced in the LR plus early FFP group at hours 8, 12, and 24 (5.23 vs. 2.07, p < 0.001; 4.49 vs. 2.05, p < 0.01; and 3.82 vs. 2.08, p < 0.05, respectively). Lactated Ringer's only groups had upregulation of Exostosin-1 and SDC-1 in the lung compared with LR plus early FFP groups ( p < 0.01 and p < 0.05) and upregulation of cytokines interluekin-10 and interferon γ ( p < 0.001 and p < 0.001). Early administration of LR plus FFP reduces the magnitude of SDC-1 shedding and dampens the cytokine response to injury. The upregulation of glycocalyx components as a response to endothelial injury is also decreased in the lung and spleen by LR plus early FFP administration.

Effects of N-Acetylcysteine on Humanin and Endostatin in Rats Exposed to Formaldehyde.

People are constantly exposed to formaldehyde, a volatile and poisonous gas, in indoor environments. In particular, anatomists, pathologists, histologists, and those involved in embalming are exposed to higher amounts of formaldehyde continuously due to their work. This study aimed to investigate the effect of N-acetylcysteine on endostatin and humanin values in male rats exposed to experimental formaldehyde. In the study, 28 male Spraque-Dawley rats aged 12-14 weeks (seven animals in each group: control group, formaldehyde group, N-acetylcysteine group, formaldehyde+N-acetylcysteine group) were used. Four weeks later, the animals were sacrificed by decapitation. Following decapitation, endostatin and humanin levels in the serum of rats were studied by the enzyme-linked immunoassay (ELISA) method. In all analyses, p<0.05 was accepted as statistically significant. Humanin and endostatin values were checked in the serum of rats. When humanin levels were compared between groups, a statistically significant difference was found between the formaldehyde group and both the control group (p<0.05) and the N-acetylcysteine group (p<0.05). In the formaldehyde+N-acetylcysteine group, it was determined that the humanin level was impaired due to formaldehyde exposure, approaching the control group values with the administered N-acetylcysteine. When the endostatin level was compared between the groups, a statistical significance (p<0.05) was found only between the formaldehyde group and the N-acetylcysteine group. In the formaldehyde+N-acetylcysteine group, it was determined that the endostatin level was impaired due to formaldehyde exposure, approaching the control group values with the administered N-acetylcysteine. In this study, the effects of N-acetylcysteine on humanin and endostatin on rats exposed to formaldehyde were demonstrated for the first time. Formaldehyde exposure negatively affected humanin and endostatin levels in rat sera. N-acetylcysteine ameliorated the negative effects of formaldehyde, bringing humanin and endostatin levels closer to the healthy control group.

Co-release of paclitaxel and encequidar from amorphous solid dispersions increase oral paclitaxel bioavailability in rats

The oral bioavailability of paclitaxel is limited due to low solubility and high affinity for the P-glycoprotein (P-gp) efflux transporter. Here we hypothesized that maximizing the intestinal paclitaxel levels through apparent solubility enhancement and controlling thesimultaneous release of both paclitaxel and the P-gp inhibitor encequidar from amorphous solid dispersions (ASDs) would increase the oral bioavailability of paclitaxel. ASDs of paclitaxel and encequidar in polyvinylpyrrolidone K30 (PVP-K30), hydroxypropylmethylcellulose 5 (HPMC-5), and hydroxypropylmethylcellulose 4 K (HPMC-4K) were hence prepared by freeze-drying. In vitro dissolution studies showed that both compounds were released fastest from PVP-K30, then from HPMC-5, and slowest from HPMC-4K ASDs. The dissolution of paclitaxel from all polymers resulted in stable concentration levels above the apparent solubility. The pharmacokinetics of paclitaxel after oral administration to male Sprague-Dawley rats was investigated with or without 1 mg/kg encequidar, as amorphous solids or polymer-based ASDs. The bioavailability of paclitaxel increased 3- to 4-fold when administered as polymer-based ASDs relative to solid amorphous paclitaxel. However, when amorphous paclitaxel was co-administered with encequidar, either as an amorphous powder or as a polymer-based ASD, the bioavailability increased 2- to 4-fold, respectively. Interestingly, a noticeable increase in paclitaxel bioavailability of 24-fold was observed when paclitaxel and encequidar were co-administered as HPMC-5-based ASDs. We, therefore, suggest that controlling the dissolution rate of paclitaxel and encequidar in order to obtain simultaneous and timed release from polymer-based ASDs is a strategy to increase oral paclitaxel bioavailability.

Kırmızı Reishi Mantarı (Ganoderma lucidum) Extratının Karbon Tetraklorür ile İndüklenen Karaciğer Hasarı ve Siklooksijenaz-2 İmmunoreaktivitesi Üzerine Etkisi

Carbon tetrachloride (CCl4) is a xenobiotic compound with toxicological action. It is absorbed by gastrointestinal system, respiratory system, and skin. Studies have reported that many countries have used Ganoderma lucidum (GL, Reishi Mushroom) as a medicinal mushroom against liver diseases induced by hepatotoxic agents such as CCl4 for more than thousands of years and is used for many diseases, including cancer since it has been thought that it increases resistance against them and treats them. In the present study, immunohistochemical localization and expression of cyclooxygenase-2 (COX-2) by administrating carbon tetrachloride and Ganoderma lucidum in adult rats were examined. In the study, 32 adult Spraque-Dawley male rats that were 8-10 weeks old were used. Rats were divided into 4 groups as control, CCI4, Ganoderma lucidum (GL), and CCI4+GL. As a result of the experimental applications, the liver tissue was found to be normal in the control and GL groups, and multifocal necrosis areas, hepatocellular degeneration, cell infiltration, sinusoidal dilatation, and congestion were observed in the central and portal areas in CCI4 group. In the CCI4+GL group, decreases were observed in lesion severity and density. COX-2 immunoreactivity was detected as more common in hepatocyte cytoplasm in the area from the central vena to the Kiernan space, while it was observed as sporadic in the hepatocyte nucleus. While CCI4 caused a decrease in total antioxidant level (TAS) in blood plasma samples, it caused an increase in total oxidant level (TOS), Aspartate aminotransferase (AST), and alanine aminotransferase (ALT) levels. It is seen that Ganoderma lucidum, which has an important place in alternative and folk medicine, reduces oxidative stress with its hepatoprotective effect and inhibits the inflammatory response in the liver.

Protective Role of Pistacia Palaestina Boiss Fruit and Leaf Extracts in Isoproterenol-Induced Cardiac Ischemia

Myocardial infarction (MI) is one of the leading causes of death worldwide. In this study aimed to investigate the protective effects of Pistacia palaestina Boiss (PP) leaf and fruit extracts, which are thought to have antioxidant and anti-inflammatory properties, in isoproterenol (ISO)-induced MI. 80 Spraque-Dawley rats were divided into 10 groups. The control group was given saline. PP leaf and fruit extracts at doses of 250 mg/kg and 500 mg/kg applied by gavage for 21 days. ISO 100 mg/kg subcutaneously was administered to the MI and MI-treatment groups on the 17th and 18th days of the experiment. Thiobarbituric acid reactive substances (TBARS) and glutathione (GSH) levels, catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities were measured in heart tissue. In serum, Troponin t, CK-MB; pro-inflammatory cytokine necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β) and IL-6; Anti-inflammatory IL-10 levels were determined by the ELISA method. Heart tissue was examined by haematoxylin-eosin staining. While lipid peroxidation indicator TBARS activity increased in the MI group, antioxidant enzyme activities and GSH levels decreased. While Troponin t, CK-MB, TNF-α, IL-1β and IL-6 levels increased, anti-inflammatory IL-10 levels decreased. Low and high dose PP leaf and fruit extracts significantly decreased TBARS, Troponin t, CK-MB, TNF-α, IL-1β, IL-6 levels, improved antioxidant enzyme activity, GSH and IL-10 levels. PP ameliorated cardiac biomarkers and histopathological changes in ISO-induced MI by suppressing oxidative stress and inflammation. PP extracts may play an important cardioprotective role in the treatment of MI with their antioxidant and anti-inflammatory effects.

LOW-DOSE THYMOQUINONE: A CHANCE FOR PREVENTIVE TREATMENT BE-FOREHEPATIC ENCEPHALOPATHY DEVELOPS: AN EXPERIMENTAL RAT STUDY

Objective: Thymoquinone (Nigella sativa), one of the popular phytotherapy bioactive sub-stances, is an antioxidant and anti-inflammatory substance with known hepatoprotective activity. In this study, we investigated whether thymoquinone has preventive effects on the development of hepatic encephalopathy in rats with hepatic encephalopathy model at two different doses. Methods: Healthy albino Spraque-dawley rats were randomized into 4 different groups: healthy negative control group, positive control group in which hepatic encephalopathy was in-duced by intraperitoneal thioacetamide 200 mg/kg, Thymoquinone 10 mg/kg and Thymoqui-none 20 mg/kg treatment groups. Thymoquinone was administered to the thymoquinone treated groups by gavage for 14 days, and then a hepatic encephalopathy model was induced with 200 mg/kg thioacetamide for three days. All rats were subjected to locomotor activity tests twice, once at the beginning and once at the end, and serum ammonium levels were measured and compared to determine whether the hepatic encephalopathy model occurred. Results: While the baseline locomotor activity tests of the groups included in the study were not statistically different, the final locomotor activity tests were found to be statistically signifi-cantly different (p&lt;0.05). In the post-hoc analysis, it was found that Thymoquinone 10 mg/kg group was statistically significantly different (p&lt;0.05) in most of the locomotor activity tests from the positive control group in which hepatic encephalopathy model was created, and on the contrary, it had similar results to the healthy negative control group (p&gt;0.05). Serum ammonium levels were lower in both thymoquinone groups compared to the positive control group, but not statistically differed (p&gt;0.05). Conclusion: Low dose Thymoquinone (10 mg/kg) group had similar results with the healthy group in both locomotor activity tests and serum ammonium levels. Thus, low dose Thymoqui-none offers a promising treatment opportunity within the scope of preventive medicine for indi-viduals at high risk of developing hepatic encephalopathy.

Unilateral Vestibulopathy Mimicking Inner Ear Ischemia Modeling Using Photothrombosis and Behavioral Assessment Using EthoVision

Objectives: Inner ear ischemic animal models using photochemical reactions have been devised in various ways. Localized vascular ischemia occurs with 532-nm laser irradiation after systemic rose bengal injection, a known photothrombotic mechanism. The aim of this study is to evaluate a photothrombosis-induced vestibulopathy mimicking behavioral changes in the inner ear ischemia model.Methods: Seven-week-old male Spraque-Dawley rats were used. Animals were divided into three groups: control group (n=6), sham laser group (n=9), and laser group (n=9). To induce the photothrombosis, animals were injected with rose bengal into the femoral vein and then were irradiated with a 532-nm laser (175 mW for 900 seconds) via transtympanic membrane. To investigate the vestibulopathy after photothrombosis, the behavior tests (tail lift reflex test, air righting reflex test, rotarod test) were performed on the 1st, 3rd, and 7th days after surgery. Additionally, an open field test was conducted and analyzed using EthoVision XT (Noldus).Results: The laser group exhibited significant behavioral change to mimic vestibulopathy in all assessments. Inducing photothrombosis with rose bengal caused severe gait instability, which precluded rotarod testing. In the tail lift reflex test, the laser group displayed vestibular dysfunction with a lower angle formation compared to the control rats. During the open field test, the laser group exhibited reduced mobility, a condition that persisted in the laser groups for 7 days.Conclusions: Noninvasive laser irradiation using rose bengal and a 532-nm laser induces photothrombosis in the inner ear of animals, leading to the development of vestibulopathy mimicking imbalanced behavior.

Effect of humanine on the Notch signaling pathway in myocardial infarction.

By applying humanin (HN) before myocardial infarction (MI), its protection in myocardial injury and the possible roles of its cellular mechanism in the Notch pathway were investigated. The study was carried out at Fırat University Experimental Research Center (12/24/2018-12/23/2019). Spraque-Dawley rats were divided into 10 groups: I (control) (n = 6), II (HN 6 h) (n = 6), III (HN 24 h) (n = 6), IV (HN day 7) (n = 6), V (MI 6 h) (n = 7), VI (MI 24 h) (n = 7), VII (MI day 7) (n = 7), VIII (MI+HN 6 h) (n = 7), IX (MI+HN 24 h) (n = 7), and X (MI+HN day 7) (n = 7). To create MI, 200 mg/kg of isoproterenol (ISO) was administered to the rats subcutaneously. Moreover, 252 μg/kg of HN was given intraperitoneally (ip) to the rats on its own and before MI. Molecular parameters Notch1, Notch2, Hes1, Hes2, Jagged1, Jagged2, DLL1, and DLL4 were examined using polymerase chain reaction in the heart tissue, Notch1, Hes1, and DLL4 were examined using western blot, while heart tissue was taken for histochemical examinations. The mRNA expression levels of the Notch signaling members (Notch1, Notch2, Hes1, Hes2, Jagged1, Jagged2, DLL1, and DLL4) tended to decrease after MI. The Notch signaling members increased more significantly, especially toward day 7 after HN application before MI. In the western blot anylyses, the Notch1, Hes1, and DLL4 protein levels increased significantly toward day 7 in the groups given HN before MI. Moreover, the serum AST, LDH, CK-MB, and troponin I levels tended to decrease with the application of HN before MI and there was a significant decrease in edema, hemorrhage, and mononuclear cells in the heart tissue at 24 h post-MI and fibrosis on day 7 post-MI. HN administration before MI has a cardioprotective effect on rats via the Notch signaling pathway.

Hepatoprotective actions of melatonin by mainly modulating oxidative status and apoptosis rate in lipopolysaccharide-induced liver damage

Aim One of the serious complications of sepsis is liver damage and liver failure. This study aimed to evaluate the protective and therapeutic potential of melatonin in rats with lipopolysaccharide-induced sepsis. Main methods Female Spraque–Dawley rats received single a dose of 7.5 mg/kg lipopolysaccharide in saline to create a 24-h sepsis model. One of the other groups received melatonin at a dose of 10 mg/kg/day beginning 1 week before sepsis induction to the end of the experiment. The melatonin group received the same doses of melatonin for the same duration but not lipopolysaccharide. The vehicle group received the same doses of saline, the vehicle of melatonin, for the same duration. Twenty-four hours after the last injection, the rats were decapitated. By appropriate histochemical, immunohistochemical, biochemical, and molecular techniques, anti-necrotic, anti-apoptotic, anti-necroptotic, anti-inflammatory, and antioxidant effects of melatonin were assessed. Key findings Lipopolysaccharide has disrupted liver functions by inducing oxidative stress, inflammation, necrotic, apoptotic, and necroptotic cell death, thus disrupting liver functions. Melatonin was found to be beneficial in terms of inhibiting the intrinsic pathway of apoptosis and tissue oxidant levels, stimulating tissue antioxidant enzyme levels, and restoring hepatocyte functions. Significance Melatonin, at those doses and duration, was found to be hepatoprotective by mainly modulating oxidative status and apoptosis rate, however, failed to significantly reduce histopathological damage. We suggest that longer-term melatonin administration may produce anti-inflammatory and anti-necrotic effects as well.

Adverse neurological effects after exposure to copper, manganese, and mercury mixtures in a Spraque-Dawley rat model: an ultrastructural investigation

ABSTRACT Exposure to environmental metal pollutants is linked to oxidative stress and the subsequent development of neurological disease. In this study, the effects of copper, manganese, and mercury, were evaluated at X100 the World Health Organization safety limits for drinking water. Using a Sprague-Dawley rat model, following exposure for 28 days, the effects of these metals on biochemical blood parameters and tissue and cellular structure of the brain were determined. Biochemical analysis revealed no hepatocellular injury with minor changes associated with the hepatobiliary system. Minimal changes were found for renal function and the Na+/K+ ratio was reduced in the copper and manganese (Cu + Mn) and copper, manganese, and mercury (Cu, Mn + Hg) groups that could affect neurological function. Light microscopy of the brain revealed abnormal histopathology of Purkinje cells in the cerebellum and pyramidal cells in the cerebrum as well as tissue damage and fibrosis of the surface blood vessels. Transmission electron microscopy of the cerebral neurons showed microscopic signs of axonal damage, chromatin condensation, the presence of indistinct nucleoli and mitochondrial damage. Together these cellular features suggest the presence and influence of oxidative stress. Exposure to these metals at X100 the safety limits, as part of mixtures, induces changes to neurological tissue that could adversely influence neurological functioning in the central nervous system.

RİFAMPİSİN KAYNAKLI BEYİN DOKUSU HASARINDA LİNALOOL’UN İYİLEŞTİRİCİ RÖLÜ

Objective&#x0D; In this study linalool (LN), which has antihyperglycemic,&#x0D; hypolipidemic and antioxidant properties, is intended&#x0D; to be used in the treatment of neurodegenerations&#x0D; and neural disorders that may occur due to rifampicin&#x0D; (RF). For this reason, it was aimed to examine the&#x0D; effects of LN on the expression of genes, biochemical&#x0D; and histopathological parameters in these metabolic&#x0D; pathways against neurotoxicity that may occur due&#x0D; to RF, and to investigate the protective effects of LN,&#x0D; which has antioxidant properties.&#x0D; Material and Method&#x0D; Thirty healthy male Spraque-Dawley rats were divided&#x0D; into five groups (group 1; control, group 2; solvent&#x0D; control (DMSO); group 3, RF; group 4, LN; group 5;&#x0D; RF+LN). Brain tissues were taken for biochemical,&#x0D; histological and gene expressions analyses. Blood&#x0D; samples were taken to measure blood glucose levels.&#x0D; Results&#x0D; Rifampicin treatment significantly increased CYP1A1&#x0D; and CYP1A2 mRNA gene expression and blood&#x0D; glucose levels, while reducing brain weight according&#x0D; to findings. On the other hand, there was a significant&#x0D; decrease in CYP1A1 and CYP1A2 mRNA gene&#x0D; expression and blood glucose levels in the RF+LN&#x0D; group, while a significant improvement in brain weight&#x0D; was observed and as a result of histological analyzes,&#x0D; it was observed that the damage caused by RF&#x0D; decreased in the groups given LN.&#x0D; Conclusion&#x0D; LN was found to be highly effective in protecting the&#x0D; brain from the toxic effects of RF.

Protective effects of sinapic acid against lead acetate-induced nephrotoxicity: a multi-biomarker approach.

Lead acetate (PbAc) is one of the top five most dangerous toxic heavy metals, particularly leading to kidney damage and posing serious health risks in both humans and animals. Sinapic acid (SNP) is a naturally occurring flavonoid found in fruits and vegetables that stands out with its antioxidant, anti-inflammatory, and anticancer properties. This is the first study to investigate the effects of SNP on oxidative stress, inflammation, apoptosis, autophagy and endoplasmic reticulum (ER) stress in PbAc-induced nephrotoxicity in rats by biochemical, molecular and histological methods. 35 Spraque dawley rats were randomly divided into five groups of 7 rats each: control, PbAc, SNP (10mg/kg), PbAc + SNP 5, PbAC + SNP 10. PbAc at a dose of 30 mg/kg body weight was administered via oral gavage alone or in combination with SNP (5 and 10 mg/kg body weight) via oral gavage for seven days. While PbAc impaired renal function by increasing serum urea and creatinine levels, SNP decreased these levels and contributed to the improvement in renal function. The administration of SNP reduced oxidative stress by increasing PbAc-induced decreased antioxidant enzyme (SOD, CAT, and GPx) activities and GSH levels, decreasing MDA levels, a marker of increased lipid peroxidation. SNP administration reduced NF-κB, TNF-α, IL-1β, NLRP3, and RAGE mRNA transcription levels, NF-κB, and TNF-α protein levels that are among the PbAc-induced increased inflammation parameters. Decreases in antiapoptotic Bcl-2 and increases in apoptotic Bax, APAF-1, and Caspase-3 due to PbAc exposure, SNP reversed the situation. SNP reduced ER stress caused by PbAc by increasing PERK, IRE1, ATF-6, CHOP, and GRP-78 levels and made it tend to regress. SNP reduced autophagy damage by decreasing the Beclin-1 protein level increased by PbAc. The findings of the present study suggested that SNP attenuates PbAc-induced nephrotoxicity.

Hesperidin ameliorates impairment in hippocampal neural stem cells related to apoptosis induced by methotrexate in adult rats

Neurogenesis is a process of generating neural stem cells (NSCs) as functional neurons can be decreased after chemotherapy treatments. Methotrexate (MTX) is a folate antagonist that is used for cancer treatment but has negative effects, including oxidative stress, neuronal apoptosis and cognitive impairments. Hesperidin (Hsd), a flavonoid found in citrus fruits, has antioxidant and neuroprotection properties. This study investigated whether Hsd could attenuate impairments of hippocampal neural stem cells related to apoptosis induced by MTX. Spraque-Dawley rats (n = 24) were divided into 4 groups: (1) Vehicle group received propylene glycol (21 days) and 0.9% normal saline (day 8 and 15), (2) Hsd group received 100 mg/kg (21 days), (3) MTX group received 75 mg/kg (days 8 and 15) and (4) MTX+Hsd group received MTX, 75 mg/kg (day 8 and 15) and Hsd 100 mg/kg (21 days). Our results showed that MTX decreased hippocampal neural stem cells including SRY (sex determining region Y)-box 2 (SOX2) and nestin. MTX diminished vascular related (VR) Ki-67 positive cells in the hippocampus but not non-vascular related (NVR) Ki-67. Additionally, MTX reduced SOX2, nestin, postsynaptic density protein 95 (PSD-95) and B-cell lymphoma-2 family of proteins (Bcl-2), whereas Bax and caspase-3 were enhanced in the hippocampal tissues. Interestingly, co-treatment with Hsd and MTX revealed upregulation of SOX2, nestin and VR Ki-67 positive cells as well as elevated SOX2, nestin, PSD-95 and Bcl-2 proteins. Moreover, receiving both Hsd and MTX significantly suppressed increased Bax and caspase-3. These results confirm that Hsd can ameliorate MTX-induced impairments of hippocampal NSC proliferation and neuronal apoptosis.

The protective effect of caffeic acid phenethyl ester in the nephrotoxicity induced by α-cypermethrin.

Alpha cypermethrin (α-CYP) is an insecticide, a member of the group of synthetic pyrethroid pesticides. This study aims to assess the histopathological and biochemical subacute effects of α-CYP on the renal tissues of 48 male Spraque-Dawley adult rats. In this study, the rats were divided into six groups: control, α-CYP (10 mg kg-1), α-CYP (20 mg kg-1), caffeic acid phenethyl ester (CAPE) (10 µmol kg-1), α-CYP + CAPE (10 mg kg-1), and α-CYP + CAPE (20 mg kg-1) groups. The percentage of weight gain was found to be dose-dependent on α-CYP in all groups. As a result of exposure, the normal histological structure of renal tissue was also observed in the control and CAPE groups, while glomerular atrophy and haemorrhage, enlargement of Bowman capsule, glomerular lobulation, and degeneration in distal and proximal tubules were noted in the α-CYP-treated groups with an increased frequency and severity in parallel with the dose increase. Although the severity and intensity of lesions decreased in the α-CYP + CAPE groups, they were statistically insignificant (p > 0.05). A decrease in the antioxidant parameter levels and an increase in oxidant parameters were observed in parallel with the negative effects of the antioxidant system in the α-CYP-treated groups. The groups exposed to CAPE in combination with α-CYP exhibited a therapeutic trend towards normalization in biochemical parameters due to the antioxidant character of CAPE. However, considering the statistical difference between the groups treated with α-CYP alone and CAPE alone, it was observed that the therapeutic features of those chemicals were not robust.

The Wound-Healing Activity of PEDOT-PSS in Animals.

This study evaluated the wound-healing activity of a polymer, Poly(3,4-ethylenedioxythiophene):poly-(styrene sulfonate) (PEDOT: PSS), and determined its mechanism based on angiogenic activity in a full-thickness excision wound model in Spraque Dawley (SD) rats. Administering PEDOT: PSS (1.6) 1.5 ppm at a dose of 50 mg/kg/day significantly improved wound healing in the SD rats on the eleventh day after the incision was created. PEDOT: PSS-treated animals presented no anti-inflammatory skin effects; however, there was an increase in angiogenic behavior. VEGF was found to be significantly elevated in the PEDOT: PSS-treated groups seven days post-incision. However, only a higher concentration of PEDOT: PSS increased TGF-β1 expression within the same time frame. Our results showed that PEDOT: PSS enhances wound healing activity, mainly in terms of its angiogenic effects. In this paper, we describe the highly conductive macromolecular material PEDOT: PSS, which demonstrated accelerated wound-healing activity in the animal incision model. The results will further provide information regarding the application of PEDOT: PSS as a dressing for medical use.

Sıçanlarda Valproik Asite Bağlı Testis Hasarına Rutin Etkisinin Araştırılması

Valproic acid (VALP) is a drug used for many psychiatric diseases such as epilepsy. However, the use of VALP has potential side effects on various tissues, including the testicles. Rutin (RUT) is a flavonoid with protective effects against oxidative stress-induced diseases and lipid peroxidation. In this study, the protective effects of RUT against testicular damage caused by VALP were investigated. For this purpose, 35 male Spraque-Dawley rats weighing 220-250 g were used in the study. The rats were randomly divided into 5 groups as Control (physiological saline), RUT (100 mg/kg/bw), VALP, (500mg/kg/bw), VALP+RUT 50 (500 mg/kg/bw VALP+50 mg/kg/bw RUT), and VALP +RUT 100 (500 mg/kg/bw VALP+100 mg/kg/bw RUT). At the end of the RUT and VALP administrations, the rats were sacrificed and testicular tissues were taken to be used for biochemical and spermatological analyzes. According to the results of this study, the MDA level in the testicular tissues of the VALP group was found to be statistically higher than the other experimental groups (p

The Effects of Carvacrol on Transient Receptor Potential (TRP) Channels in an Animal Model of Parkinson's Disease.

In this study, we aimed to investigate the effects of carvacrol (CA), a widely used phytochemical having anti-oxidant and neuroprotective effects, on transient receptor potential (TRP) channels in an animal model of Parkinson's disease (PD). A total of 64 adult male Spraque-Dawley rats were divided into four groups: sham-operated, PD animal model (unilateral intrastriatal injections of 6-hydroxydopamine (6-OHDA), 6µg/µl), PD + vehicle (dimethyl sulfoxide (DMSO)) treatment, and PD + CA treatment (10mg/kg, every other day, for 14days). Half of the brain samples of substantia nigra pars compacta (SNpc) and striatum (CPu) were collected for immunohistochemistry and the remaining half were used for molecular analyses. CA treatment significantly increased the density of dopaminergic neurons immunolabeled with tyrosine hydroxylase and transient receptor potential canonical 1 (TRPC1) channel in the SNpc of PD animals. In contrast, the density of astrocytes immunolabeled with glial fibrillary acetic acid and transient receptor potential ankyrin 1 (TRPA1) channel significantly decreased following CA treatment in the CPu of PD animals. RT-PCR and western blot analyses showed that 6-OHDA administration significantly reduced TRPA1 and TPRPC1 mRNA expression and protein levels in both SNpc and CPu. CA treatment significantly upregulated TRPA1 expression in PD group, while TRPC1 levels did not display an alteration. Based on this data it was concluded that CA treatment might protect the number of dopaminergic neurons by reducing the reactive astrogliosis and modulating the expression of TRP channels in both neurons and astrocytes in an animal model of PD.

Investigation of the effect of Polygonum cognatum Meissn. ethanol extract Bax, Caspase-3, Bcl-2, NF-B and NRF-2/HO-1 pathways in streptozotocin induced diabetic rats

In this study, it was investigated of the effect of Polygonum cognatum Meissn. ethanol extract Bax, Bcl-2, Caspase-3, NF-kB and NRF-2/HO-1 pathways in streptozotocin induced diabetic rats. A total of 24 healthy Spraque-Dawley male rats were randomly divided into four groups containing of 6 rats per group as Control; Diabetes mellitus (DM); Polygonum cognatum Meissn. ethanol extract (PCE) and DM+PCE. Experimental diabetes was induced by a single dose of 60 mg/kg/i.p Streptozotocin (STZ) injection for DM and DM+PCE groups. The animals showing diabetes (Blood glucose level &gt;250 mg/dL) will be selected for diabetes groups in 7 th days. PCE was given at a dose of 10 mg/kg /day/p.o via gavage 20 days. All of rats were sacrificed on 20 th day, taken blood and dissected kidney tissues ender anesthesia. Bax, Bcl-2, Caspase-3, COX-2, HO-1, NF-kB and Nrf-2 expression levels were determined by western blotting in kidney tissue. Compared with the control and diabetes groups, Bax, Caspase-3, COX-2 and NF-kB expression levels increased (p&lt;0.001); Bcl-2, HO-1 and Nrf-2 expression levels were decreased in diabetes group. PCE given with STZ decreased Bax, Caspase-3, COX-2 and NF-kB expression levels (p&lt;0.001); Bcl-2, HO-1 and Nrf-2 expression levels were increased. PCE treats STZ-induced diabetic kidney injury by regulating apoptosis parameters such as Bax, Bcl-2, Caspase-3, and inflammation pathways such as, NF-kB, COX-2, Nrf-2 and HO-1 against STZ-induced diabetes. It was concluded that PCE can be used as a therapeutic agent after determining the molecular processes behind the therapeutic benefits of PCE against kidney damage in STZ-induced diabetes. kidney injury kidney damage. According to the biochemical findings, PCE 10 mg/kg treatment dose decreased in kidney Bax Bcl-2, Caspase-3 and NF-kB pathways, increased in kidney Nrf-2 and HO-1 protein expression levels when administered with STZ was presented as a pioneering study in the literature.

Adverse effects of copper, manganese and mercury, alone and in mixtures on the aorta and heart of Spraque-Dawley rats.

Cardiovascular diseases (CVD) are a common global cause of death and are therefore a major health concern. Inhaled or ingested environmental heavy metals contribute to the development of CVD. The aim of this study was to address the limited information available on the effect of relevant dosages of metals in mixtures. Three metals with reported effects on the cardiovascular system (CVS) were identified, and these metals were copper (Cu), manganese (Mn) and mercury (Hg). In Sprague-Dawley rats, the adverse effects of copper (Cu), manganese (Mn) and mercury (Hg), alone and as part of mixtures, on the blood parameters, the aorta and heart were investigated. Forty-eight male Sprague-Dawley rats were randomly divided into eight groups (n = 6): control, Cu, Mn, Hg, Cu + Mn, Cu + Hg, Mn + Hg and Cu, Mn + Hg. The seven experimental groups received the metal mixtures at 100 times the World Health Organisation (WHO) safety limit for drinking water (2mg/L for Cu, 0.4mg/L for Mn and 0.06mg/L for Hg) via oral gavage for 28days. After 28days, compared with the control, red blood cell levels were increased for Cu + Hg. All other measured blood parameters were unchanged. Morphological changes in the tunica media were connective tissue deposition and an abundance of collagen type I in the metal exposed aortic tissues. In the cardiac tissue of metal-exposed rats, changes in the cardiomyocyte and myofibrillar arrangement, with an increase in collagen type I and III was observed. Ultrastructurally, the aortic collagen and elastin band arrangement and the cardiac mitochondrial and myofibrillar arrangement and structures were altered in the experimental groups. These changes indicated that exposure to these metals in rats caused minor changes in the blood parameters, however, the changes in tissue and cellular structure indicated an increased risk for the development of CVD.