Damage In Sprague-Dawley Rats Research Articles

Increased Sperm DNA Damage in Sprague-Dawley Rats Exposed to Dextromethorphan as an Antitussive

Introduction: Male reproductive functions have been observed to be negatively impacted by the antitussive dextromethorphan (DM). It was also discovered that DM has an impact on micronutrients (such as zinc, calcium, and selenium) which are crucial for both capacitation and the acrosome reaction, which can result in infertility. Using Sprague-Dawley rats as models, we investigated the effects of quercetin and rutin on DM-induced toxicity in males in relation to apoptotic protein markers. Methodology: For a period of 16 weeks, 80 male rats, weighing 150 ± 30 g, were utilized and split into four groups. Twenty animals were employed in each group. For a period of 16 weeks, Group B received 20 mg/kg, Group C received 40 mg/kg, and Group D received 80 mg/kg of DM. Group A acted as the control group and received 1 ml of distilled water (DW). Five randomly chosen animals from each group were put to sleep at the end of the DM treatment period, and their testes were taken out to measure DNA fragmentation using comet assay. To ascertain the pace of recovery, the animals were then split into three groups, E–G, and kept for a total of 16 weeks. Group G received 1 ml of DW, Group F was given rutin (25 mg/kg), and Group E was given quercetin (50 mg/kg). Results: Comparing DM-treated groups to control revealed a significant dose-dependent decrease in DNA fragmentation. When DM-treated and recovery-alone groups were contrasted with rutin and quercetin groups, an improvement in DNA was seen. Conclusion: Significant improvements in the parameters were observed when rutin and quercetin supplements were used, which may lessen the harmful effects of DM and enhance male fertility.

Protective effect of intermittent hypobaric hypoxia against radiation-induced liver damage in Sprague-Dawley rats.

Without timely and effective interventions or treatments, radiation-induced liver damage (RILD) can lead to serious consequences for the patients and their families. To investigate the protective effect of intermittent hypobaric hypoxia preconditioning (IHHP) in RILD. Male adult SD rats were randomly divided into 8 groups including one control group, one only irradiation group and other experimental groups. Blood routine tests and liver function tests were all assessed with abdominal venous blood. Moreover, hematoxylin eosin (HE) staining and immunohistochemistry assay were used to detect the histopathological changes and expressions of transforming growth factor-β1 (TGF-β1), tumor necrosis factor α (TNF-α) and hypoxia-inducible factor 1α (HIF-1α) in radiated liver sections. Blood routing tests showed that RBC, WBC and Hb were all significantly increased while the differences of these results between different groups with same simulated altitude were approximate. However, liver function in the IHHP plus irradiation at 4000 m group was significantly decreased (P< 0.05) compared to only irradiation groups, and the manifestation of HE and lower positive expression of TNF-α showed improved histopathological changes in the liver section. Furthermore, no significant difference of HIF-1α expression between any two groups treated with IHHP was observed. IHHP at the altitude of 4000 m group could alleviate the radioactive liver damage by downregulating TNF-α and less strong positive expression of TGF-β1. Furthermore, patients exposed to radiation might benefit from this treatment to prevent or reduce the RILD.

Retraction: The Gastroprotective Effect of Vitex pubescens Leaf Extract against Ethanol-Provoked Gastric Mucosal Damage in Sprague-Dawley Rats.

Retraction: The Gastroprotective Effect of Vitex pubescens Leaf Extract against Ethanol-Provoked Gastric Mucosal Damage in Sprague-Dawley Rats.

GC–MS analysis, and evaluation of protective effect of Piper chaba stem bark against paracetamol-induced liver damage in Sprague-Dawley rats: Possible defensive mechanism by targeting CYP2E1 enzyme through in silico study

The present study attempted to scrutinize the protective effect of the methanolic extract of P. chaba stem bark against paracetamol-induced hepatotoxicity in Sprague−Dawley rats, along with the gas chromatography–mass spectrometry (GC–MS) analysis to identify phytochemicals, which were further docked in the catalytic site of CYP2E1 and the MD simulation for system that plays a major role in the bio-activation of toxic substances that produce reactive metabolites, leading to hepatotoxicity. P. chaba stem methanol extract (250 and 500 mg/kg) were treated orally with the negative control and the negative control silymarin (50 mg/kg) groups. Phytochemical profiling was conducted using GC–MS. In in-silico studies, PyRx software was used for docking analysis and the stability of the binding mode in the target active sites was evaluated through a set of standard MD-simulation protocols using the Charmm 27 force field and Swiss PARAM. Co-administration of P. chaba at both doses with APAP significantly reduced the APAP-augmented liver marker enzymes ALT, AST, ALP, and LDH, along with serum albumin, globulin, hepatic enzymes, histopathological architecture, lipid profiles, total protein, and total bilirubin, and elevated the levels of MDA. The GC–MS analysis indicated that P. chaba extract is enriched in fatty acid methyl esters (46.23 %) and alkaloids (10.91 %) and piperine is represented as a main phytochemical. Among all the identified phytochemicals, piperine (−8.0 kcal/mol) was found to be more interacting and stable with the binding site of CYP2E1. Therefore, all of our findings may conclude that the P. chaba stem extract and its main compound, piperine, are able to neutralize APAP-induced hepatic damage.

Preventive Effect of Limosilactobacillus fermentum SCHY34 on Lead Acetate-Induced Neurological Damage in SD Rats

Lead poisoning caused by lead pollution seriously affects people's health. Lactic acid bacteria has been shown to be useful for biological scavenging of lead. In this experiment, Sprague-Dawley (SD) rats were treated with 200 mg/L of lead acetate solution daily to induce chronic lead poisoning, and oral Limosilactobacillus fermentum (L. fermentum) SCHY34 to study its mitigation effects and mechanisms on rat neurotoxicity. The L. fermentum SCHY34 showed competent results on in vitro survival rate and the lead ion adsorption rate. Animal experiments showed that L. fermentum SCHY34 maintained the morphology of rat liver, kidney, and hippocampi, reduced the accumulation of lead in the blood, liver, kidney, and brain tissue. Further, L. fermentum SCHY34 alleviated the lead-induced decline in spatial memory and response capacity of SD rats, and also regulated the secretion of neurotransmitters and related enzyme activities in the brain tissue of rats, such as glutamate (Glu), monoamine oxidase (MAO), acetylcholinesterase (AchE), cyclic adenosine monophosphate (cAMP), and adenylate cyclase (AC). In addition, the expression of genes related to cognitive capacity, antioxidation, and anti-apoptotic in rat brain tissues were increased L. fermentum SCHY34 treatment, such as brain-derived neurotrophic factor (BDNF), c-fos, c-jun, superoxide dismutase (SOD)1/2, Nuclear factor erythroid 2-related factor 2 (Nrf2), and B-cell lymphoma 2 (Bcl-2), and so on. L. fermentum SCHY34 showed a great biological scavenging and potential effect on alleviating the toxicity of lead ions.

Protective effect of GYY4137, a water‑soluble hydrogen sulfide‑releasing molecule, on intestinal ischemia‑reperfusion.

The present study aimed to clarify the protective effects of p‑methoxyphenyl morpholino‑phosphinodithioic acid (GYY4137), a water‑soluble hydrogen sulfide‑releasing molecule, on a rat model of intestinal ischemia‑reperfusion (IIR). A total of 40 healthy male Sprague Dawley (SD) rats were randomly divided into four groups (n=10/group): Group A, a sham‑surgery group; Group B, the IIR group; group C, rats with IIR that were administered an abdominal injection of low‑dose GYY4137 (40mg/kg); and group D, rats with IIR that were administered high‑dose GYY4137 (80mg/kg). Intestinal histomorphology was observed using hematoxylin and eosin staining, and the concentrations of malondialdehyde (MDA) and superoxide dismutase (SOD) were measured. Apoptotic index (AI) was determined by terminal deoxynucleotidyl‑transferase‑mediated dUTP nick end labeling. Reverse transcription‑quantitative PCR analysis was performed to assess the expression levels of intestinal caspase‑3, Bax and Bcl‑2. Notably, disordered arrangement of intestinal villi and mucosal necrosis were detected in group B, which was substantially improved by GYY4137 treatment (groups C and D). MDA content (nmol/mg) was 2.83±0.36, 9.23±0.78, 4.97±0.45 and 3.51±1.05nmol/mg in groups A, B, C and D, respectively. In addition, SOD concentration (U/mg) was 135.37±3.34, 76.45±1.39, 95.13±1.64 and 115.13±2.54 in groups A, B, C and D, respectively. Furthermore, AI in group B (21.73±1.17%) was markedly higher than that in group A (4.53±0.28%) and in the GYY4137 intervention groups (9.53±0.96 and 6.53±0.76% in groups C and D, respectively). Compared with in group A, the mRNA expression levels of Bax and caspase‑3 were markedly higher in group B (P<0.05), whereas the expression of Bcl‑2 was significantly lower (P<0.05). Furthermore, compared with in group B, Bcl‑2 expression was higher, and Bax and caspase‑3 expression was lower in groups C and D (P<0.05). In conclusion, GYY4137 may alleviate IIR‑induced damage in SD rats.

Minocycline protects against acrylamide-induced neurotoxicity and testicular damage in Sprague-Dawley rats.

This study investigated the protective effects of minocycline against acrylamide (ACR)-induced neurotoxicity and testicular damage in Sprague-Dawley rats. Forty rats were divided into five groups (eight rats each). Group I received saline (0.5 mL/rat) daily for 10 days and served as the untreated control group. Group II received ACR (30 mg/kg body weight (b.w.)) daily for 10 days. Group III received ACR (30 mg/kg b.w.) daily for 10 days and subsequently minocycline (60 mg/kg b.w.) for five days. Group IV received ACR (30 mg/kg b.w.) daily for 10 days followed by saline for five days and served as the control group for the ACR-minocycline-treated group. Group V received minocycline (60 mg/kg b.w.) for five days. All treatments were administered orally. Rats in group I and V showed normal locomotor behavior and normal histology of the brain and testes. Administration of ACR (Group II and IV) resulted in weight loss and gait abnormalities. Furthermore, neuronal degeneration in the hippocampus and cerebellum and degeneration of the seminiferous tubular epithelium with formation of spermatid giant cells were observed. Ultrastructurally, ACR specifically damaged spermatogonia and spermatocytes. Acrylamide was also seen to cause a significant increase of malondialdehyde levels in the brain and testes. Treatment of ACR-administered rats with minocycline (Group III) significantly alleviated the loss of body weight and improved locomotor function. Minocycline also ameliorated neuronal degeneration and seminiferous tubular damage and decreased malondialdehyde concentrations. In conclusion, minocycline protects against neurotoxic effects of acrylamide and seminiferous tubular damage. Decreasing lipid peroxidation by minocycline might play a role in such protection.

Role of the gene Phlda1 in fenvalerate-induced apoptosis and testicular damage in Sprague-Dawley rats

ABSTRACTFenvalerate (FEN), a pyrethroid insecticide used worldwide, has been shown to produce a potentially adverse effect on male reproduction. However the mechanisms are not completely understood. Thus this study aimed to (1) determine whether cellular apoptosis was involved in FEN-induced testicular damage in rats, and (2) identify the potential mechanism involved in FEN-induced apoptosis in testes. Data demonstrated that FEN markedly decreased serum testosterone levels, increased the inner diameter of seminiferous tubules, decreased the layers of spermatogenic cells, disturbed spermatogenesis and increased the number of apoptotic cells. Further, bioinformatic analysis of gene microarray in rat testis tissue showed that FEN significantly altered the expressions of genes (Krt8, Mal, Cd24, Lcn2, Phlda1, Arg2) related to apoptotic related processes. The expression pattern of these 6 genes was upregulated in FEN-treated rat testicular tissue. qRT-PCR analysis demonstrated that Phlda1, a well-documented pro-apoptotic factor, was significantly elevated by FEN. The expression of PHLDA1 testicular protein was also elevated following FEN exposure. In conclusion, our results suggest that FEN exposure induced deleterious effects on rat testes associated with Phlda1-mediated apoptosis which may act as a molecular mechanism underlying FEN induced rat testicular damage.

The Role of Astragaloside IV against Cerebral Ischemia/Reperfusion Injury: Suppression of Apoptosis via Promotion of P62-LC3-Autophagy.

Background: Ischemia/reperfusion (I/R) caused by ischemic stroke treatments leads to brain injury, and autophagy plays a role in the pathology. Astragaloside IV is a potential neuroprotectant, but its underlying mechanism on cerebral I/R injury needs to be explored. The objective of this study is to investigate the neuroprotective mechanism of Astragaloside IV against cerebral I/R injury. Methods: Middle cerebral artery occlusion method (MCAO) and oxygen and glucose deprivation/reoxygenation (OGD/R) method were used to simulate cerebral I/R injury in Sprague-Dawley (SD) rats and HT22 cells, respectively. The neurological score, 2,3,5-Triphe-nyltetrazolium chloride (TTC) staining, and transmission electron microscope were used to detect cerebral damage in SD rats. Cell viability and cytotoxicity assay were tested in vitro. Fluorescent staining and flow cytometry were applied to detect the level of apoptosis. Western blotting was conducted to examine the expression of proteins associated with autophagy. Results: This study found that Astragaloside IV could decrease the neurological score, reduce the infarct volume in the brain, and alleviate cerebral I/R injury in MCAO rats. Astragaloside IV promoted cell viability and balanced Bcl-2 and Bax expression in vitro, reduced the rate of apoptosis, decreased the expression of P62, and increased the expression of LC3II/LC3I in HT22 cells after OGD/R. Conclusions: These data suggested that Astragaloside IV plays a neuroprotective role by down-regulating apoptosis by promoting the degree of autophagy.

Abstract P193: Anti-fibrotic and Anti-oxidant Actions of a Muscadine Grape Extract Supplement on Hypertension-induced Cardiac Damage

Approximately 75 million U.S. adults suffer from hypertension, an independent risk factor for pathological cardiac hypertrophy. The current study examines the effects of a muscadine grape extract formulation (MGE; Piedmont Research &amp; Development Corp.) with anti-oxidant, anti-inflammatory, and anti-proliferative properties on hypertension-induced cardiac damage in Sprague-Dawley rats receiving a 4-week Ang II infusion (24 μg/kg/h). We previously showed that MGE in the drinking water had no effect on blood pressure or systolic function in normotensive or hypertensive rats; however, MGE ameliorated the Ang II-induced decrease in diastolic function and increase in cardiomyocyte cross-sectional area. In the current study, MGE supplementation of Ang II-treated rats decreased interstitial cardiac fibrosis, reducing collagen III staining in the myocardium (0.9 ± 0.2% control, 6.8 ± 1.0% Ang II, and 2.8 ± 0.4% Ang II/MGE; p&lt;0.01). MGE alone had no effect on any parameters assessed. The positive correlation between collagen and diastolic function with Ang II compared to control (p&lt;0.01) was significantly abrogated by co-administration of MGE. TGFβ is a critical cytokine that stimulates cardiac fibrosis. The Ang II-mediated increase in cardiac TGFβ mRNA was attenuated by MGE (relative gene expression: 1.0 ± 0.1 control, 2.0 ± 0.4 Ang II, 1.1 ± 0.2 Ang II/MGE; p&lt;0.05) as was downstream pSmad2 protein in cardiomyocytes (% nuclei: 26.1 ± 6 control, 53.8 ± 9.6 Ang II, 27.6 ± 5.5 Ang II/MGE; p&lt;0.05) and cardiac fibroblasts (2.3 ± 1.1 control, 11.7 ± 4.9 Ang II, 2.2 ± 0.5 Ang II/MGE; p&lt;0.05). NADPH oxidase is a primary contributor to cardiac oxidative stress and excess ROS production can lead to activation of pro-fibrotic pathways. MGE significantly reduced the Ang II-induced increase in p22phox mRNA (relative gene expression: 1.0 ± 0.1 control, 1.9 ± 0.1 Ang II, 1.0 ± 0.1 Ang II/MGE; p&lt;0.0001) and protein (relative density: 1.0 ± 0.2 control, 5.4 ± 1.6 Ang II, 2.9 ± 1.0 Ang II/MGE; p&lt;0.05), a subunit required for NADPH oxidase activity. These results indicate that MGE ameliorates cardiac fibrosis by targeting NADPH oxidase and the TGFβ pro-fibrotic pathway, suggesting that MGE supplementation may be an effective, natural therapeutic for hypertension-induced cardiac damage.

Effects of Wearing Bio-active Material Coated Fabric against γ-irradiation-induced Cellular Damage in Sprague-Dawley Rats

Background: Ionizing radiation causes cellular damage and death through the direct damage and/or indirectly the production of ROS, which induces oxidative stress. This study was designed to evaluate the in vivo radioprotective effects of a bio-active material coated fabric (BMCF) against γ-irradiation-induced cellular damage in Sprague-Dawley (SD) rats. Materials and Methods: Healthy male SD rats wore bio-active material coated (concentrations in 10% and 30%) fabric for 7 days after 3 Gy of γ-irradiation. Radioprotective effects were evaluated by performing various biochemical assays including spleen and thymus index, WBC count, hepatic damage marker enzymes [aspartate transaminase (AST) and alanine transaminase (ALT)] in plasma, liver antioxidant enzymes, and mitochondrial activity in muscle. Results and Discussions: Exposure to γ-irradiation resulted in hepatocellular and immune systemic damage. Gamma-irradiation induced decreases in antioxidant enzymes. However, wearing the BMCF-30% decreased significantly AST and ALT activities in plasma. Furthermore, wearing the BMCF-30% increased SOD (superoxide dismutase) and mitochondrial activity. Conclusion: These results suggest that wearing BMCF offers effective radioprotection against γ-irradiation-induced cellular damage in SD rats.

The Gastroprotective Effect of Vitex pubescens Leaf Extract against Ethanol-Provoked Gastric Mucosal Damage in Sprague-Dawley Rats.

Vitex pubescens is a Malaysian therapeutic plant employed in traditional drug to remedy a variety of disorders. The purpose of this research is to assess the gastroprotective efficiency of V. pubescens leaves against ethanol-induced gastric hemorrhagic laceration in rats. Animals were randomly allocated into seven groups and pre-treated, separately, with 10% Tween 20 (normal and ulcer control groups), 20 mg/kg omeprazole (reference group), and 62.5, 125, 250, and 500 mg/kg of V. pubescens extract (experimental groups). All animals were sacrificed after another hour. Histological evaluation of the ulcer control group revealed significant injury to the gastric mucosa with edema and leucocyte infiltration of the submucosal layer. PAS staining, showed remarkably intense magenta color, remarkable increase of HSP70 and decrease of Bax proteins in rats pre-treated with plant extracts compared to the ulcer control group. Gastric homogenates revealed a remarkable increase in endogenous antioxidant enzyme activities (CAT, SOD, GSH) and a decrease in the lipid peroxidation level (MDA) in animals pre-treated with V. pubescens extract compared with the ulcer control group. The gastroprotective activity of this plant might be related to increased antioxidant enzymes and decrease lipid peroxidation upsurge of HSP70 and reduced expression of Bax proteins

Development of quercetin-phospholipid complex to improve the bioavailability and protection effects against carbon tetrachloride-induced hepatotoxicity in SD rats

Quercetin (QT) is a natural flavonoid with various biological activities and pharmacological actions. However, the bioavailability of QT is relatively low due to its low solubility which severely limits its use. In this study, we intended to improve the bioavailability of QT by preparing quercetin-phospholipid complex (QT-PC) and investigate the protective effect of QT-PC against carbon tetrachloride (CCl4) induced acute liver damage in Sprague-Dawley (SD) rats. The physicochemical properties of QT-PC were characterized in terms of infrared spectroscopy (FTIR), differential scanning calorimetry (DSC), powder X-ray diffraction (XRPD) and water/n-octanol solubility. FTIR, DSC and XRPD data confirmed the formation of QT-PC. The water solubility of QT was improved significantly in the prepared complex, indicating its increased hydrophilicity. Oral bioavailability of QT and QT-PC was evaluated in SD rats, and the plasma QT was estimated by HPLC-MS. QT-PC exhibited higher Cmax (1.58±0.11 vs. 0.67±0.08μg/mL), increased AUC0–∞ (8.60±1.25 vs. 2.41±0.51mg/Lh) and t1/2z (7.76±1.09 vs. 4.81±0.87h) when compared to free QT. The greater absorption of QT-PC group suggested the improved bioavailability. Moreover, biochemical changes and histopathological observations revealed that QT-PC provided better protection to rat liver than free QT at the same dose. Thus, phospholipid complexation might be one of the suitable approaches to improve the oral bioavailability of QT and obtain better protective effects against CCl4 induced acute liver damage in SD rats than free QT at the same dose level.

Prophylactic effects of thymoquinone against carbon tetrachloride-induced hepatic damage in Sprague-Dawley rats

This study is conducted to investigate the prophylactic effect of thymoquinone (TQ), the major active ingredient of Nigella sativa seeds, against carbon tetrachloride (CCl4)-induced hepatic damage in Sprague-Dawley (SD) rats. Forty rats were divided into four even groups. The first group served as control. The second, third and fourth groups received CCl4, CCl4 and TQ, and TQ only, respectively for 5 weeks. CCl4 (2 ml/kg b.w.) was given orally by gastric tube twice a week on Sunday and Thursday. TQ (20 mg/kg b.w.) was given daily in corn oil by gastric tube. At the end of the experiment, rats were sacrificed, and blood samples and liver specimens were obtained for biochemical analysis and morphological examination, respectively. Control and TQ-treated rats showed normal serum activity for alanine (ALT) and aspartate (AST) aminotransferases, and normal liver histology. Treatment of rats with CCl4 significantly increased serum activity of ALT and AST aminotransferases compared to control rats. Histopathologically, livers from CCl4-treated rats showed dilatation of blood sinusoids and portal blood vessels, Kupffer cell activation, vacuolar degeneration of hepatocytes, focal areas of necrosis and mild hepatic fibrosis. Using transmission electron microscopy (TEM), CCl4 caused clear lesions in the liver including dilatation of endoplasmic reticula, increased extracellular matrix and formation of abundant fatty globules and numerous autophagosomes in hepatocytes. On the other hand, co-administration of TQ with CCl4 significantly decreased serum ALT and AST activities, and attenuated most of CCl4-induced hepatic pathological changes. The present study indicates that TQ has the potential to attenuate CCl 4-induced hepatic damage in SD rats.

Efficacy Study of Livartho against Paracetamol Induced Hepatotoxicity in Adult Sprague Dawley Rats

Liver disease is a worldwide problem. It is an exposed to many kinds of xenobiotics and therapeutic agents. The purpose of this study was to evaluate therapeutic effect of Livartho drug in paracetamol induced hepatic damage Sprague dawley rats. Paracetamol at the dose level of 900mg/kg body weight administered through intraperitoneal route once daily for one week to produced liver damage in rats as manifested by the significantly decrease body weight and feed consumption along with significantly increase liver organ weight and serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), total bilirubin, cholesterol and triglyceride and decrease the total protein and albumin levels along with significantly increase myloperoxidase enzyme activity, lipid peroxidation and protein carbonyl levels as compared to control group. The antioxidant parameters such as reduced glutathione (GSH), oxidized glutathione (GSSG), total thiol and GSH/ GSSG ratio were also found lowered in paracetamol treated group as compared with control. After treatment with Livartho drug (206.6 mg/kg body weight) once daily for 16 days to paracetamol treated rats shows significantly lowered the afore mentioned biochemical parameter whereas protein and albumin levels were increased along with significant increased above mentioned antioxidant enzymatic parameters. The results of this study strongly indicate that Livartho drug is most effective medicine which has potent hepatoprotective action and free radical scavenger against paracetamol induced hepatic damage in Sprague dawley rats.

Protective Effect of the Gastrodiae Rhizoma-gamibang on the Scopolamine-induced Hippocampal Damage in Sprague-Dawley Rats

Objectives : This study investigated the neuroprotective effect of Gastodia Rhizoma-gamibang (GG) water extracts against scopolamine-induced neurotoxicity in the hippocampus of male Sprague-Dawley rats. Methods : The animals were divided into five different groups with six a nimals per each group. The normal group (Nor) was administered with saline, while the control gro up (Con) was administered with saline after scopolamine treatment. The experimental group (Exp) was administered orally GG extracts at doses of 200 ㎎/㎏ (GG1 group), 400 ㎎/㎏ (GG2 group), 1000 ㎎/㎏ (GG5 group) for 30 day after scopolamine treatment. Results : From a light microscopy study, the nuclei of neurons and glial cells in the hippocampus were more shrunken or condensed in the 30 day control group compared with normal group. In the experimental groups, proportional to the dose, recovered from neurotoxicity induced by scopolamine. The control group, the density of hippocampal neurons were reduced 17-20% compared to normal group. The densities of neurons from the CA1, and CA3 area of the hippocampus in the GG1, GG2 and GG5 groups significantly increased compared with the Con. In the experimental group, neuronal cells are recovered from scopolamine-induced damage. A number of glial cells are observed increase from GG2 and GG5 groups. The PAS-positive materials in the tissues hippocampus), was lower in the Exp than the Con. Conclusions : The present study demonstrates that Gastodia Rhizoma-gamibang extract reduces neuronal damage in the hippocampus of scopolamin-induced impairment mice.

The role of the hippocampus in avoidance learning and anxiety vulnerability.

The hippocampus has been implicated in anxiety disorders and post-traumatic stress disorder (PTSD); human studies suggest that a dysfunctional hippocampus may be a vulnerability factor for the development of PTSD. In the current study, we examined the effect of hippocampal damage in avoidance learning, as avoidance is a core symptom of all anxiety disorders. First, the effect of hippocampal damage on avoidance learning was investigated in outbred Sprague Dawley (SD) rats. Second, the function of the hippocampus in Wistar-Kyoto (WKY) rats was compared to SD rats. The WKY rat is an animal model of behavioral inhibition, a risk factor for anxiety, and demonstrates abnormal avoidance learning, marked by facilitated avoidance acquisition and resistance to extinction. The results of the current study indicate that hippocampal damage in SD rats leads to impaired extinction of avoidance learning similar to WKY rats. Furthermore, WKY rats have reduced hippocampal volume and impaired hippocampal synaptic plasticity as compared to SD rats. These results suggest that hippocampal dysfunction enhances the development of persistent avoidance responding and, thus, may confer vulnerability to the development of anxiety disorders and PTSD.

Carbon tetrachloride (CCl4)-induced hepatic damage in experimental Sprague Dawley rats: Antioxidant potential of Xylopia aethiopica

The present study was carried out to evaluate the hepatoprotective effects of aqueous extract of Xylopia aethiopica stem bark (XASB) on carbon tetrachloride (CCl4) induced liver damage in sprague dawley rats. Experimental rats were randomly divided into four groups of five rats each. Group 1: served as the control rats, Group 2: was administered with CCl4 only in groundnut oil (1:1) at a dose of 3 ml/kg b.wt by single intraperitoneal administration. Group 3: was administered with extract of X. aethopica + CCl4 ( 250 mg/kg b.wt/day) , Group 4: was treated with extract of X. aethiopica + CCl4 ( 500 mg/kg b.wt/day).Serum alanine transferase (ALT), aspartate amino transferase (AST) and alkaline phosphatase (ALP) levels 24 hrs after CCl4 administration decreased significantly (p≤0.05) in rats pretreated with X. aethiopica than in CCl4-treated rat only. Total serum bilirubin also showed a remarkable decrease in rats pretreated with xylopia aethiopica when compared to those administered with CCl4 alone. The activities of GST and CAT in liver tissues were increased in the rats pretreated with X. aethiopica compared with CCl4 alone. Lipid peroxidation expressed by malondialdehyde (MDA) concentration was significantly decreased (p≤0.05) in rats pretreated with X. aethiopica compared with CCl4 treated rat. However, the rats pretreated with X. aethiopica showed significant improvements in the cytoarchitecture of rat liver. The results suggested that aqueous extract of X. aethopica could palliate the liver injuries perhaps by its antioxidative effect, hence eliminating the deleterious effect of toxic metabolites from the CCl4.

Nephroprotective and Curative Assessment of an Aqueous Seed Extract of Parkia clappertoniana Keay in Gentamicin-induced Renal Damage in Sprague-dawley Rats

Aim: To assess the nephroprotective and curative effects of an aqueous seed extract of Parkia clappertoniana on gentamicin-induced renal damage (GIRD) in Sprague-Dawley rats. Study Design: Experimental Place and Duration of Study: Department of Medical Laboratory, University of Cape Coast, Ghana between September, 2012 and May 2013. Methodology: In assessing nephro protective effect, rats were pretreated (10 days) with P. clappertoniana aqueous seed extract (1-2 g kg; p.o) prior to induction of renal damage by treatment with gentamicin (0.08g kg; p.o, for 8 days. Serum biochemical markers (Creatinine, Urea, Na and K) and urine parameters (leukocyte, protein, specific gravity and pH) of renal damage were determined and compared with baseline values. In a curative study, GIRD in rats was treated with Normal Saline (2 ml kg; p.o), Losartan Original Research Article European Journal of Medicinal Plants, 4(2): 234-248, 2014 235 (0.05 g kg; p.o), or extract (1-2 g kg; p.o) for 14 days and serum and urine parameters determined for all treatments. Histopathology and changes in kidney weights for normal and treated rats in both studies were assessed. The extract was screened for DPPH radical scavenging activity. Results: The extract significantly (P ≤ .001) reduced elevated serum creatinine and urea secondary to GIRD (P ≤ .05) and significantly (P ≤ .05) reduced elevated serum Na but had no effect on K. Elevated urine proteins and leucocytes secondary to GIRD was significantly (P ≤ .05) reduced; but had no significant effect on urine pH and specific gravity. Elevated kidney weights associated with GIRD was significantly (P≤ .01) reduced. Histopathological assessment revealed healing effect by extract to GIRD. Effects of the extract were similar to Losartan. Pretreatment with extract however had no significant effect on GIRD as serum and urine parameters, as well as kidney weights were significantly (P≤ .01) elevated on induction of renal damage. Conclusion: The aqueous seed extract of Parkia clappertoniana has curative but no nephroprotective effect on gentamicin-induced renal damage in Sprague-Dawley rats.

Short-term administration of an aqueous extract of kalanchoe integra var. crenata (Andr.) Cuf leaves produces no major organ damage in Sprague-Dawley rats

Ethnopharmacological relevanceKalanchoe intergra (Ki) leaf extract is an orally administered multipurpose plant medicine in Ghana and other parts of the world for the treatment of ulcers, pain and adenoma of the prostate gland. There is paucity of information concerning its short-term usage. The present study is aimed at conducting histopathological and biochemical studies in a 14-day sub-acute toxicity studies using female Sprague-Dawley rats. Materials and methodsCrude extract of Ki leaves was prepared and freeze-dried. A 14-day sub-acute toxicity studies was conducted using 2 week old nulliparous and non-pregnant female Sprague-Dawley rats (120–150g). Reconstituted Ki was administered at a dosage of 900mgkg−1 (high dose), 300mgkg−1 with a control group receiving an equivalent volume of distilled water (as vehicle) by gastric lavage. Histopathological studies of major organs and blood chemistry analysis were performed on blood obtained via cardiac puncture into EDTA tubes after euthanisation. ResultsThere was a significant decrease in urea (p<0.016) and creatinine levels (p<0.001) in both the high and low dose groups. There was an increase in ALP levels (P=0.01) in both the high and low dose groups. ALT and AST rather decreased significantly in both the high and low dose groups (p<0.0001). Histopathological results did not show any abnormalities in all the H&E stained paraffin sections. Thus the photomicrographs of the liver, kidney and heart were within histopathological limits. ConclusionKi leaf extract is non-toxic when administered by the oral route over a time period of 14 days at the above doses.