Rats In Treatment Group Research Articles

Effects of bone marrow-derived mesenchymal stem cells on the autophagic activity of alveolar macrophages in a rat model of silicosis.

The aim of the present study was to evaluate the effects of bone marrow-derived mesenchymal stem cells (BMSCs) on the expression of the autophagy-associated proteins, microtubule-associated protein light chain 3 (LC-3) and autophagy-related gene Beclin-1 (Beclin-1), in alveolar macrophages (AMs) in a rat model of silicosis. Furthermore, the study investigated the molecular mechanisms underlying the effects of BMSC treatment. A population of 60 adult female Sprague-Dawley (SD) rats were allocated at random into three groups, namely the control, model and BMSC treatment groups (n=20 per group). BMSCs were isolated from five male SD rats (age, 6-8 weeks) and cultured in vitro. The silicosis model was established using a single 1.0-ml infusion of silicon dioxide suspension administered via non-exposed tracheal intubation. Rats in the BMSC treatment group received a 1.0-ml transplantation of BMSCs (1×106/ml). The rats were sacrificed on days 1, 7, 14 and 28 after modeling, and AMs were extracted from the rats using bronchoalveolar lavage. Third-generation BMSCs were identified using flow cytometry with fluorescein isothiocyanate staining, and the morphological characteristics of the AMs were observed using hematoxylin and eosin staining. The expression levels of LC-3 and Beclin-1 were determined using immunocytochemistry sand western blot analysis. The expression levels of LC-3 and Beclin-1 were found to be increased at all the time points in the model group. LC-3 and Beclin-1 levels began to increase at day 1, peaked at day 14 and decreased after day 28; however, the levels remained elevated compared with the basal expression levels. The AMs of the BMSC treatment group exhibited significantly alleviated pathological symptoms compared with the model group AMs, as indicated by significantly decreased expression levels of LC-3 and Beclin-1 at each time point. Therefore, the results indicated that autophagy was promoted in the AMs of the silicosis model rats. Furthermore, treatment with BMSCs was demonstrated to reduce the expression levels of LC-3 and Beclin-1, subsequently inhibiting autophagic activity and mitigating the damage associated with silicosis.

Sweet Dream Liquid Chinese Medicine Ameliorates Learning and Memory Deficit in a Rat Model of Paradoxical Sleep Deprivation through the ERK/CREB Signaling Pathway.

Sweet dream oral liquid (SDOL), a traditional Chinese herbal compound contains 17 traditional Chinese medicines. It has various pharmacological effects, such as improving brain dysfunction and increasing sleeping quality. This study investigated the neuroprotective effect and the underlying mechanisms of SDOL-impaired hippocampus learning and memory-induced paradoxical sleep deprivation (PSD) in rats. Sixty Male Wistar rats were randomly divided into six groups. Before PSD, SDOL treatment group rats were intragastrically administered SDOL for 25 days at dose of 2.1, 4.2, and 8.4 mL/kg body weight per day. Normal control group, large platform control group, and PSD groups were treated with normal saline instead of SDOL. After 25 days treatment, PSD and SDOL groups were deprived of paradoxical sleep for 72 h. Then two behavioral studies were conducted to test the spatial learning and memory ability using the open field test and Morris water maze test. Expression of the c-fos, c-jun, cyclic AMP response element binding protein (CREB), extracellular signal-regulated protein kinase (ERK), mitogen-activated protein kinases (MAPK)/ERK kinase (MEK), and p-CREB, p-ERK, and p-MEK in the hippocampus were also assayed by western blot. In this study, PSD decreased the levels of p-CREB, p-ERK, p-MEK, c-fos, and c-jun. However, SDOL treatment increased expressions of these proteins. Our results showed that SDOL improved 72-h PSD-induced cognitive impairment. These affects may be mediated by increasing the contents of c-fos, c-jun, and p-CREB/ERK signaling.

Protective effect of Allicin on intestinal mucosal barrier of septic rats

Objective To investigate the protective effect of allicin on intestinal mucosal barrier of septic rats so as to explore the possible mechanism. Methods Twenty-four male SD rats were randomly (random number)divided into sham, septic model and allicin treatment group. Septic model was established by cecal ligation and puncture (CLP) in rats. Rats in the treatment group were administered with allicin (30 mg/kg, ip) at 6 h and 12 h after modeling, while those in the model and sham groups were treated with equal amount of saline instead. Rats were sacrificed at 24 h and the serum D-lactic acid, diamine oxidase (DAO) and fluorescence isothiocyanate-dextran (FITC-Dextran, FD-40) were determined to evaluate the intestinal mucosal barrier function. The levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), malondialdehyde (MDA), and the activity of superoxide dismutase (SOD) in intestinal tissue were measured. Histopathological changes of intestinal mucosa injury were assessed by Hematoxylin-eosin staining. Results Compared with the sham group, levels of serum D-lactic acid, DAO and FD-40 increased significantly in the CLP group (D-lactic acid: 599.4±101.1 vs. 149.2±20.63 nmol/mL, t=11.84, P<0.01; DAO: 302.1±64.5 vs. 76.57±14.76 ng/mL, t=9.433, P<0.01; FD-40: 6664.0±1437.0 vs. 1446.0±205.0 ng/mL, t=9.704, P<0.01); intestinal morphology damage occurred in the CLP group; intestinal levels of TNF-α, IL-6 and MDA increased greatly (TNF-α: 186.35±20.43 vs. 58.76±8.94 pg/mL, t=17.23, P<0.01; IL-6: 763.25±85.23 vs. 125.36±14.37 pg/mL, t=22.54, P<0.01; MDA: 29.36±3.27 vs. 7.24±0.85 nmol/mg prot, t=16.61, P<0.01), while SOD activity reduced (35.75±6.53 vs. 73.26±8.35 U/mg prot, t=10.57, P<0.01) in the CLP group. Allicin treatment greatly inhibited the increase of D-lactic acid, DAO and FD-40 levels in rat plasma caused by CLP (D-lactic acid: 330.1±81.77 vs. 599.4±101.1 nmol/mL, t=7.086, P<0.01; DAO: 171.8±49.70 vs. 302.1±64.56 ng/mL, t=5.45, P<0.01; FD-40: 3349.0±1167.0 vs. 6664.0±1437.0 ng/mL, t=6.165, P<0.01); intestinal morphology damage was improved in the allicin treatment group; allicin treatment greatly inhibited the intestinal levels of TNF-α, IL-6 and MDA and preserved the intestinal SOD activity compared with the CLP group (TNF-α: 95.37±12.68 vs. 186.35±20.43 pg/mL, t=12.29, P<0.01; IL-6: 354.27±46.27 vs. 763.25±85.23 pg/mL, t=14.45, P<0.01; MDA: 16.27±3.14 vs. 29.36±3.27 nmol/mg prot, t=9.831, P<0.01; SOD: 55.35±6.23 vs. 35.75±6.53 U/mg prot, t=5.522, P<0.01). Conclusions Allicin could inhibit local inflammation and oxidative stress in the intestine and exerts protective effect on intestinal mucosal barrier of septic rats. Key words: Allicin; Sepsis; Intestinal mucosal barrier; D-lactic acid; Diamine oxidase; Fluorescein isothiocyanate-dextran; Inflammation; Oxidative stress

Anti-proliferative and Apoptotic Effects of Basella rubra (L.) Against 1, 2-Dimethyl Hydrazine-induced Colon Carcinogenesis in Rats.

Colorectal cancer is a very prevalent diagnosed cancer. The current study was performed in order to examine the role of BRAE (Basella rubra aqueous extract) in regulating aberrant crypt foci (ACF) formation, cell proliferation and inhibition of apoptosis in a colon carcinogenesis model in male Wistar rats. Rats were randomly allocated into six groups. Group I served as control, and group II acted as a drug control administered BRAE (250mg/kg b.w.) orally for 30 weeks. Rats in group III-VI were given subcutaneous injections of DMH (25mg/kg b.w. weekly) for 15 weeks to initiate colon carcinogenesis. Those in group IV and VI were administered BRAE along with DMH injections. Rats in group V were administered with BRAE after cessation of DMH injection. After 30 weeks of experimental period colons were obtained from experimental groups and analyzed for ACF incidence, argyrophilic nucleolar organizing region- associated proteins (AgNOR) count, histopathological and immunohistochemical changes. Only in DMH exposed groups were ACF and AgNOR numbers increased. Administration of BRAE appreciably decreased the numbers of ACF and AgNOR in BRAE treated groups. Histopathological findings revealed a high level of dysplastic changes with decreased number of goblet cells found only in only DMH injected rats. Administration of BRAE in treated group rats reversed these changes. Expression markers for cell proliferation (PCNA and Ki67) were elevated in DMH treated rats, but reduced with BRAE treatement. This expression was reversed with apoptosis markers (p53 and Caspase-3). Thus the results results of the present study were found to be significant and confirmed the potential efficacy of BRAE against colon carcinogenesis.

Formulation and in vivo evaluation of oro-dispersible tablets of ayurvedic powders Sitopaladi and Talisadi

Most of the ayurvedic medicines are in the form of powder and they may have some kind of unacceptable or bitter taste and have problem of patient compliance. Medicines in powder form have problem of administration of accurate dose with ease. Furthermore it needs water or honey for administration and chances of spoilage and waste are more. Formulation of Oro-dispersible tablets which rapidly disintegrate in mouth will be the best remedy for efficient use of ayurvedic powders. The aim of this study was to formulate oro-dispersible tablets of ayurvedic polyherbal powder Sitopaladi and Talisadi using various excipients like super-disintegrants and sweeteners and compare the efficacy in vivo using rats. The cough suppressing activities of powder and tablets was evaluated by counting bouts of cough in control group and treated group rats with powders and ODT. Codeine was taken as standard anti-tussive drug for our research. The cough bouts were produced in rats by exposure to SO2 generated by reaction of Na2SO3 and water in a Desiccator. The test results show that there is very little change in the activity of formulated tablets and pure ayurvedic powder. Thus it can be concluded from the study that that formulation of oro-dispersible tablets of ayurvedic powder preparation not only results in improving acceptability, ease and accuracy of administration without affecting efficiency of powder ayurvedic preparations like Talisadi and Sitopaladi.

T-2 toxin induced nephrotoxicity in Wistar rats

The present experiment was designed to elucidate nephrotoxicity induced by feeding of graded doses of T-2 toxin in Wistar rats. A total of 192 male Wistar rats, 4 weeks of age were used for the study and were divided into four groups of 48 rats each receiving different levels of T-2 toxin in feed i.e. groups I-0.5 ppm, II-0.75 ppm and III-1.0 ppm and group IV (control) toxin free diet. The duration of the experiment was 12 weeks and 8 animals each were sacrificed at 2, 4, 6, 8, 10 and 12 weeks intervals. Biochemically, increased levels of BUN and serum creatinine were observed in T-2 treated group rats. Significant increase in oxidative stress enzymes like MDA and decrease in SOD, Catalase and GSH in kidneys potentiated the role of free radicals in causing renal injury in T-2 toxicity. Pathomorphological studies revealed gross changes in kidneys viz, pale, soft and moderately enlarged in a dose and duration dependent manner. The relative weights of kidneys were increased in T-2 treated rats as compared with those in controls. The most consistent histopathological lesions in the kidneys included swollen and vacuolated epithelial cells of PCTs, occasional necrosis with presence of proteinaceous/cellular casts in the lumen along with congestion of intertubular blood vessels, mononuclear cell infiltration in interstitium, swollen parietal epithelial cells of Bowman's capsule and dilatation of DCTs which were more conspicuous at later stages. It was concluded that oxidative stress plays a major role in T-2 toxin induced nephrotoxicity.

Tetradecyl 2,3-dihydroxybenzoate promotes functional recovery after spinal cord injury in adult rats.

Tetradecyl 2,3-dihydroxybenzoate (ABG001) is a small molecule separated from gentian extract that has a similar effect to nerve growth factor. It is not clear whether it can promote functional recovery in animals suffering from a central nervous system injury. In order to explore the role of ABG001 in restoration of tissue structure and motor function of rats with spinal cord injury (SCI), ABG001 (0.4 mg/kg) was administered intraperitoneally. Subsequently, behavioral assessments and morphological studies were performed to detect recovery of hind limb motor function and neuroregeneration. The results showed that compared with DMSO group, the rats in the ABG treatment group had better performance in BBB score and grip strength test (P < 0.05), the area of necrosis was smaller (P < 0.05), GFAP expression was significantly reduced (P < 0.01), and Map-2 expression was significantly increased (P < 0.01). Additionally, after ABG treatment, the number of fluorogold positive cells transported reversely to red nucleus increased (P < 0.05). The results suggest that ABG001 can promote recovery of hind limb motor function in rats with SCI, which may be related to its functions of inhibiting glial cell proliferation and promoting neuroregeneration.

Antioxidant and hepatoprotective effects of fermented red ginseng against high fat diet-induced hyperlipidemia in rats.

This study was performed to investigate the antioxidant and hepatoprotective effects of fermented red ginseng (Panax ginseng C.A. Meyer; FRG) on high-fat diet-induced hyperlipidemia in rats. Sprague-Dawley rats were divided into four groups of seven: normal control, NC; high-fat diet control, HFC; high-fat diet–0.5% FRG, HF-FRGL; and high-fat diet–1% FRG, HF-FRGH. All rats were fed a high-fat diet for eight weeks, except those in the NC group, while rats in the FRG treatment groups received drinking water containing 0.5% or 1% FRG. After eight weeks of treatment, levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total cholesterol (TC), triglycerides (TG), low-density lipoprotein-cholesterol (LDL-C), and high-density lipoprotein-cholesterol (HDL-C) in the serum were measured. The concentration of the oxidative stress marker malondialdehyde (MDA), and activity of antioxidant enzymes including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) in rat liver were evaluated. Histological analysis of the liver was performed using hematoxylin and eosin. The high-fat diet markedly increased serum levels of ALT, AST, TC, TG, and LDL-C and hepatic MDA levels, while administration of FRG to the hyperlipidemic rats resulted in a significant decline in the levels of these parameters. Furthermore, the decline in the levels of serum HDL-C and hepatic SOD, CAT, and GSH-Px induced by the high-fat diet was attenuated by FRG treatment. In addition, histopathological analysis of liver sections suggested that FRG treatment also provided protection against liver damage. These results suggested that FRG improved lipid profiles, inhibited lipid peroxidation, and played a protective role against liver injury in hyperlipidemic rats.

Role of Ginseng as Hepatoprotective, Antioxidant and Anti-Inflammatory against Methotrexate Induced Liver Injury in Rats.

Background Ginseng, an ancient and famous medicinal herb in the Orient, has been used as a valuable tonic and for the treatment of various diseases including hepatic disorders. Ginseng extracts and individual ginsenosides have shown a wide array of beneficial role in the regulation of regular liver functions and the treatment of liver disorders. Objective: This study tries to determine the hepatoprotective , antioxidant and anti-inflammatory effects of ginseng on Methotrexate (MTX)-induced hepatotoxicity Materials and Methods: forty rats (weigh 150-180 g) were used. The rats were kept in animal house for one week and had access to water and food . Temperature was kept at 37 °C. After one week, the rats were randomly divided into four equal groups: Group (A) (control) received normal saline ; group (B )received Ginseng(1.8 ml/kg/day) orally ; group( C) received MTX (100 μg/kg) intraperitoneally and group (D) received MTX (100 μg/kg) intraperitoneally with ginseng (1.8 ml/kg/day) orally. After six weeks, the rats were decapitated and evaluation of liver function was done. Results: Ginseng treatment markedly suppressed the serum alanine aminotransferase (ALT) , aspartate aminotransferase (AST) and serum gama glutamil transpeptidase (λGTP) activiteis . Ginseng was attributed to stimulate anti-oxidant protein contents, such as glutathione peroxidase (GPX). The marked increase of proinflammatory cytokines ( TNF α ) in MTX treated rats group was additionally attenuated by ginseng, Conclusion : Ginseng effectively prevent liver injury, mainly through down regulation of oxidative stress and inflammatory response.

Role of Lycopersicon esculentum in diethylnitrosamine-induced and phenobarbital-promoted hepatocellular carcinoma

Objective: This study aims to evaluate the role of Lycopersicon esculentum in diethylnitrosamine (DEN)-induced and phenobarbital (PB)-promoted hepatocellular carcinoma. Materials and Methods: The hepatocarcinogenesis was induced in male Wistar albino rats by DEN (single injection, 200 mg/kg, i.p . ); 2 weeks later, 0.05% w/v of PB was administered through drinking water for 16 weeks. The treatment group rats received a similar dosage as above along with enzymatic extract of L. esculentum (250 mg/kg body weight p.o.) at 3 rd week onward. The carcinogenesis was evaluated by estimating biochemical markers such as alanine transaminase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP), and bilirubin, DNA and RNA levels, liver protein, and cancer biomarkers as alpha-fetoprotein (AFP). Results: Treatment with enzymatic extract of L. esculentum significantly reduced DEN/PB-mediated elevation of ALT, AST, ALP, and bilirubin levels. A significant decrease in the levels of DNA, RNA, and AFP and increase in liver protein were observed when L. esculentum -treated rats were compared with DEN/PB-treated rats. Conclusion: The present study suggests that L. esculentum possesses chemopreventive activity against DEN-induced and PB-promoted liver cancer.

Pharmacological evaluation of Mallotus philippinensis (Lam.) Muell.-Arg. fruit hair extract for anti-inflammatory, analgesic and hypnotic activity.

Objective:Recently, we observed wound healing activity of 50% ethanol extract of Mallotus philippinensis Muell. Arg (MP) fruit hairs extract (MPE). In several intestinal infections, localized inflammation is of common occurrence and hence we evaluated the anti-inflammatory, analgesic and hypnotic activity of MPE in different rat experimental models.Materials and Methods:Anti-inflammatory activity was evaluated by carrageenan (acute) and turpentine oil induced formalin (subacute) induced paw edema and while granuloma pouch (subacute) in rats. Analgesic and hypnotic activity of MPE was undertaken by tail-flick, hot-plate, and acetic acid-induced writhing tests while pentobarbitone-induced hypnotic potentiation in rats.Results:MPE at a dose of 200 mg/kg at 3 h after their administration showed inhibition of formalin-induced paw edema by 41.60% (P < 0.001) and carrageenan-induced paw edema by 55.30% (P < 0.001). After 7 days of treatments, MPE showed 38.0% (P < 0.001) inhibition against formalin-induced paw edema and reduced weight of turpentine-induced granuloma pouch by 29.6% (P < 0.01) and volume of exudates by 26.1% (P < 0.01), respectively. MPE (200 mg/kg) showed dose-dependent elevation in pain threshold and peak analgesic effect at 120 min as evidenced by increased latency period in tail flick method and increased reaction time in the hot-plate test while the reduction in the number of acetic acid-induced writhes by 45.7% (P < 0.001). The pentobarbitone-induced hypnosis model showed potentiation, as defined by increased duration of sleep in treated group rats as compared to control.Conclusion:Thus, the study revealed MPE is effective in reducing acute and subacute inflammation and showed effective and similar analgesic activity. This seemed to be safe in the treatment of pain and inflammation.

Melatonin Activates Endoplasmic Reticulum Stress and Apoptosis in Rats with Diethylnitrosamine-Induced Hepatocarcinogenesis.

Hepatocellular carcinoma (HCC) is one of the most lethal human cancers worldwide because of its high incidence, its metastatic potential and the low efficacy of conventional treatment. Inactivation of apoptosis is implicated in tumour progression and chemotherapy resistance, and has been linked to the presence of endoplasmic reticulum stress. Melatonin, the main product of the pineal gland, exerts anti-proliferative, pro-apoptotic and anti-angiogenic effects in HCC cells, but these effects still need to be confirmed in animal models. Male Wistar rats in treatment groups received diethylnitrosamine (DEN) 50 mg/kg intraperitoneally twice/once a week for 18 weeks. Melatonin was given in drinking water at 1 mg/kg/d, beginning 5 or 12 weeks after the start of DEN administration. Melatonin improved survival rates and successfully attenuated liver injury, as shown by histopathology, decreased levels of serum transaminases and reduced expression of placental glutathione S-transferase. Furthermore, melatonin treatment resulted in a significant increase of caspase 3, 8 and 9 activities, polyadenosine diphosphate (ADP) ribose polymerase (PARP) cleavage, and Bcl-associated X protein (Bax)/Bcl-2 ratio. Cytochrome c, p53 and Fas-L protein concentration were also significantly enhanced by melatonin. Melatonin induced an increased expression of activating transcription factor 6 (ATF6), C/EBP-homologous protein (CHOP) and immunoglobulin heavy chain-binding protein (BiP), while cyclooxygenase (COX)-2 expression decreased. Data obtained suggest that induction of apoptosis and ER stress contribute to the beneficial effects of melatonin in rats with DEN-induced HCC.

Calcium fluoride nanoparticles induced suppression of Streptococcus mutans biofilm: an in vitro and in vivo approach.

Biofilm formation on the tooth surface is the root cause of dental caries and periodontal diseases. Streptococcus mutans is known to produce biofilm which is one of the primary causes of dental caries. Acid production and acid tolerance along with exopolysaccharide (EPS) formation are major virulence factors of S. mutans biofilm. In the current study, calcium fluoride nanoparticles (CaF2-NPs) were evaluated for their effect on the biofilm forming ability of S. mutans in vivo and in vitro. The in vitro studies revealed 89 % and 90 % reduction in biofilm formation and EPS production, respectively. Moreover, acid production and acid tolerance abilities of S. mutans were also reduced considerably in the presence of CaF2-NPs. Confocal laser scanning microscopy and transmission electron microscopy images were in accordance with the other results indicating inhibition of biofilm without affecting bacterial viability. The qRT-PCR gene expression analysis showed significant downregulation of various virulence genes (vicR, gtfC, ftf, spaP, comDE) associated with biofilm formation. Furthermore, CaF2-NPs were found to substantially decrease the caries in treated rat groups as compared to the untreated groups in in vivo studies. Scanning electron micrographs of rat's teeth further validated our results. These findings suggest that the CaF2-NPs may be used as a potential antibiofilm applicant against S. mutans and may be applied as a topical agent to reduce dental caries.

Effect of Preservation Methods of Oil Palm (Elaeis guineensis) Sap on Health Status of Male Wistar Rats

Male Wistar rats (30) which were split into five groups of six rats each were administered four different forms of oil palm tree (Elaeis guineensis) sap samples by gavage based on 1.5% of their weekly body weights. The group 1 which served as control received only water, group 2 received pasteurized palm sap (PPS), group 3 received market palm wine (MPW), and group 4 received frozen palm sap (FPS), whereas group 5 received fresh palm sap (FrPS). Chemical compositions of the sap samples were determined. Normal feed and water were fed ad libitum. The mean body weight and feed intake of each rat group was measured every three (3) days. Blood samples were collected weekly for determination of random and fasten blood glucose. After 2 months of treatment, the bloods of each male rat group samples were collected for determination of the liver and kidney functions, while the palm sap products were subjected for microbial analyses. The sap samples content were analysed [1]. The palm sap was evaluated for its effect on the mean body weight and vital organ weight of albino rats. Results showed that palm sap had effect in reducing the mean body weight of the exposed rat groups compared to the control which could be attributed to the low alcohol content and probiotic effect of the fresh palm sap on the treated rat group. The spleen and kidney of the control rat group showed significant decrease compared to the treated rat groups, while the liver of the rat groups could be compared favourably. The percentage increases observed in spleen and kidney of the exposed rat groups was attributed to the presence of alcohol in the palm sap. However, since the liver of the palm sap treated rat groups were comparable to the control; it showed that the presence of alcohol in the palm sap administered to the Wistar rats were within normal limits. There were no significant differences on the random and fasting blood glucose of the rats which is an indication that palm sap drinking may not elevate the blood glucose levels in the blood stream. Results obtained also showed that palm sap contained mainly Saccharomyces cerevisiea. However, the presence of Citrobacter freundi in the MW could be associated with adulteration or exposure to unhygienic environment.

E-cadherin expression in a rat model of acute pancreatitis.

A clinical requirement exists for early biomarkers that can predict the severity of acute pancreatitis (AP). In order to determine whether E-cadherin is associated with the severity of AP, a pancreatitic rat model was established and the expression levels of E-cadherin were detected. A study population of 24 Sprague Dawley rats was administered intraperitoneal injections of various concentrations of L-arginine in order to induce pancreatitis. Rats were assigned to the severe acute pancreatitis (SAP) or mild acute pancreatitis (MAP) group based on the results of histological evaluations and the serum levels of amylase. An additional 8 rats received intraperitoneal injections of NaCl solution, as a control group. For each group, the serum concentrations of soluble E-cadherin and the expression levels of E-cadherin protein in the pancreatic tissue were detected. The results indicated that the rat model of pancreatitis was successfully established. Rats in the high concentration L-arginine treatment group, which exhibited a higher pancreatitis pathology score and level of serum amylase, were assigned to the SAP group. Low concentration L-arginine group rats were assigned to the MAP group. The pathology scores and levels of serum amylase in the SAP and MAP group rats were higher compared with the control group rats. The levels of serum E-cadherin were the most elevated in the SAP group. Statistically significant differences were detected in the SAP and MAP groups compared with the control group, and in the SAP group compared with the MAP group (P<0.05). Furthermore, the levels of E-cadherin protein in the pancreatic tissue were elevated in the SAP group compared with the MAP and control groups. In conclusion, the present study demonstrated that E-cadherin was overexpressed in SAP rats, and the overexpression of E-cadherin may be associated with the severity of AP.

Gene expression profiling and inhibition of adipose tissue accumulation of G. bimaculatus extract in rats on high fat diet.

BackgroundMolecular genetic mechanisms underlying the anti-inflammatory effects of ethanol extract (GB) from G. bimaculatus, a type of cricket, are not fully elucidated. G. bimaculatus was reported to be rich in unsaturated fatty acid and to decrease the omega-6/omega-3 fatty acid ratio when fed to chickens. GB may reduce the amount of fat or increase the unsaturated fatty acid ratio.MethodsMale Wistar rats fed a high-fat diet (HFD) were orally administered with 5 groups: phosphate buffered saline (PBS, control), GB (100 mg/kg or 200 mg/kg), Pravastatin or Isaria sinclairii (IS) extract, which is reported to have fat-reducing effects, for either 1 or 2 months. GB’s sero-biochemial, hematological and anti-oxidizing hepato-cellular biomarker levels were evaluated to dertermine their antilipidemic, anti-inflammatory, and anti-coagulant effect in rats after 1 or 2 month GB treatments on HFD (fat 60 %) Wistar rat. The abdominal and epididymidal fat weight were measured and the composition of fatty acid was analyzed by GC/MS. Microarray analyses were performed with a rat 28 K cDNA clone set array to identify the gene-expression profiles for the GB exposed high fat dieted Wistar rat.ResultsThe weight and fatty acid composition of abdominal fat and epididymidal fat, total cholesterol, LDL-cholesterol, and triglyceride in GB treated rats were at lower levels than those of the control group. The anti-oxidant hepato-cellular biomarker levels, protein carbonyl content and malondialdehyde concentration in GB treated rats were significantly decreased. Compared to the control, the GB treated rat group (treated at a dose of 100 and 200 mg/kg), had 190 up-regulated genes including Gpm6a (glycoprotein m6a), Tmem14a (transmembrane protein 14A) and Fasin (fatty acid synthase), with down-regulated 235 genes including Cc121b (chemokine ligand 21b), Glycan1 (glycosylation dependent cell adhesion moleule, Serpinb1a (serine proteinase inhibitor) and Tcrb (T-cell receptor beta chain).ConclusionThe data suggest Fasin-related fatty acid synthesis and adipose differentiation related protein (Adfp), which is related to obesity, were upregulated by GB treatment, indicating their potential therapeutic markers for anti-atheriosclerosis or inflammation.

Emilia coccinae (SIMS) G Extract improves memory impairment, cholinergic dysfunction, and oxidative stress damage in scopolamine-treated rats.

BackgroundE. coccinae (SIMS) G. (Asteraceae) is an annual plant commonly found throughout the plain of the Central Africa and widely used in Cameroonian folk medicine for the treatment of fever and convulsions in children. We previously reported that the methanolic extract of this plant improved spatial memory. However no underlying mechanism was explored. The present study was undertaken to investigate the effects of the hydroalcoholic extract of Emilia coccinae on memory in scopolamine treated rats and to propose possible mechanisms of action.MethodsNovel object recognition and Y-maze paradigm were used to test memory while oxidative profile, AChE and ACh level of the whole brain were assessed to outline the mechanism of nootropic activity of the extract. 200 and 400 mg/kg of the extract were chronically administrated during 14 consecutive days in separate groups of scopolamine intraperitoneal treated rats (1.5 mg/kg).ResultsThe hydroalcoholic extract of Emilia coccinae (HEEC) at the dose of 200 mg/kg significantly improved the memory of rats and reversed the amnesia induced by scopolamine. In addition, we showed that this extract is decreasing the acetyl cholinesterase activity while also increasing the acetylcholine levels in the brain. HEEC (200 and 400 mg/kg) significantly increased antioxidant enzyme activities (SOD, GSH and CAT) and reduced lipid peroxidation (MDA level) in the rat whole brain homogenates.ConclusionsTaken together, our results suggested that the hydroalcoholic extract of Emilia coccinae ameliorated the cognitive dysfunction in scopolamine treated rats through the blockage of the oxidative effect of scopolamine and inhibition of AChE activity.

English

The aim of wound care is to promote wound healing in the shortest time possible, and plants are a great source of medicines, especially in traditional medicine. Traditionally, medicinal plants have been used for many years as topical and internal preparations to promote wound repair. This work will give an overview of twelve West Africa medicinal plant studies and their active phytochemicals in direct wound healing. The process of wound healing is promoted by several herbal extracts, which are composed of active agents like triterpenes, alkaloids, flavonoids, tannins, saponins, anthraquinones, and other biomolecules. 55% of overviewed plants contain tannins and we found that 45% of them contain terpenoids. Saponins are present at a level of 36% in these overviewed plants. Finally, we remarked that 80% of plants studied here contain flavonoids. The antioxidant and anti-inflammatory activities of flavonoids were believed to be one of the important mechanisms in wound healing and in the presence of tannin it improved the regeneration and organization of the new tissue and hastened the wound healing process. Sterols and polyphenols are also responsible for wound healing due to free radical-scavenging and antioxidant activity, which are known to reduce lipid peroxidation. Cactus extract up-regulates VEGF expression in wounded skin, stimulating in return angiogenesis for supplying nutrients and oxygen for skin regrowth. The expression of MMPs revealed the enhanced healing pattern in the E. guineensis leaf extract treated rats group. In conclusion, biochemically wound healing process is promoted by active agents in herbal extracts and those components act synergistically. Key words: Medicinal plants, phytochemicals, biochemically wound healing.

Restoration of erectile function with intracavernous injections of endothelial progenitor cells after bilateral cavernous nerve injury inrats.

Endothelial progenitor cells (EPCs) are bone marrow-derived endothelial cells capable of circulating, proliferating, and differentiating into mature endothelial cells. Circulating EPCs can be directly recruited to some extent at sites of injury, and their administration could accelerate repair or endothelialization of the damaged tissue. We investigated the effects of intracavernous injections of EPCs into the corpora cavernosa of rats with erectile dysfunction (ED) caused by bilateral cavernous nerve (CN) injury. Overall, 24 male Sprague-Dawley rats were randomized into three groups: sham surgery, vehicle-only, or EPC treatment. Rats in the EPC treatment and vehicle-only groups were subjected to bilateral CN injury before injection of EPCs or vehicle, respectively, into the corpora cavernosa. Four weeks after surgery, erectile function was assessed by measuring maximum intracavernosal pressure (ICP), change in ICP, area under the ICP curve, and ratio of change in ICP and mean arterial pressure (MAP; ΔICP/MAP). Penile tissue was histomorphometrically analyzed for the expression of neural nitric oxide synthase (nNOS), neurofilament-1 (NF-1), von Willebrand factor (vWF), endothelial NOS (eNOS), and smooth muscle cell content. Maximum ICP and all other functional parameters of erectile function were significantly reduced in the vehicle-only group vs. the sham and EPC treatment groups (all p<0.001). Smooth muscle cell content was decreased in the vehicle-only vs. the sham and EPC treatment groups (both p<0.01). Expressions of vWF and eNOS in the dorsal artery were significantly higher in the EPC treatment than the vehicle-only group (p<0.05). In conclusion, EPC treatment restored erectile function in a rat model of bilateral CN injury through recruitment of EPCs toward the dorsal artery and preservation of smooth muscle cells in the corpus cavernosum. These findings elucidate the therapeutic potential of EPCs for treating ED in humans.

Lycopene has reduced renal damage histopathologically and biochemically in experimental renal ischemia-reperfusion injury

Background: The present study aimed to investigate whether the inflammatory and antioxidant lycopene has a therapeutic effect against renal ischemia/reperfusion (I/R) injury. Materials and methods: In this study, 24 Wistar-Albino rats, weighing from 200 to 250 g, were divided into four groups. All rats underwent median laparotomy under anesthesia. No procedures were performed in the control group (Group C), whereas 100 mg/kg lycopene was administered by gavage in the lycopene group (Group L). The arteries of both kidneys were clamped for 45 min in the ischemia group (Group I), whereas 100 mg/kg lycopene was administered by gavage 30 min before clamping renal arteries, and ischemia was performed in the treatment group (Group T) rats. For all rats, blood samples and renal tissues were collected at 6 h of reperfusion. Samples were used to examine serum BUN, creatinine, MDA and GSH levels, and the renal tissues were used to examine MDA and GSH levels, and renal histopathologies. Results: The treatment group had statistically significant lower serum MDA levels, histopathological tubular vacuolization, loss of brush border and tubular dilatation (p < 0.05), whereas serum BUN, creatinine, tissue MDA, and tissue and serum GSH levels were improved in favor of the treatment group, even though it was not statistically significant (p > 0.05). Conclusion: The present study demonstrated that lycopene, which was administered prior to renal I/R injury, prevented renal damage through biochemical and histopathological parameters.