Regular Rat Diet Research Articles

Cardioprotection of Water Spinach (Ipomoea aquatica), Wood Apple (Limonia acidissima) and Linseed (Linum usitatissimum L.) on Doxorubicin-Induced Cardiotoxicity and Oxidative Stress in Rat Model.

The aim of this study was to investigate the pharmacological efficacy of 3 functional foods (Water spinach, Wood apple, and Linseed) against doxorubicin-induced cardiotoxicity and oxidative stress in rat models. Twenty-five Wistar Albino rats (male and female) were equally classified into 5 groups. Except for the normal control (NC) group, the animals received 2.5 mg/kg doxorubicin (DOX) intra-peritoneal injection at 48 hours intervals to create a dose of 15 mg/kg overall for 14 days. Simply a standard diet was given to the NC and DOX groups. In the 3 treatment groups such as water spinach (DOX + WS), wood apple (DOX + WA), and linseed (DOX + LS), rats were given 14 gm/day/rat fried water spinach, mashed wood apple, roasted linseed, respectively mixed with regular rat diet at 1:1 ratio. Blood and heart samples were collected by sacrificing all the rats on the last of the experiment day (the 15th day). LDH (lactate dehydrogenase), CK-MB (creatine kinase myocardial band), MDA (malondialdehyde), and SOD (superoxide dismutase) were analyzed. Additionally, histopathological analysis was conducted for final observation. The functional foods were indicated to lower the serum cardiac biomarkers (LDH and CK-MB) as well as stress marker (MDA) significantly (P < .05) and improved heart function and oxidative stress. However, the change in serum SOD level was noted as statistically insignificant (P > .05). The biochemical outcomes of the food intervention groups were supported by the histological findings found in those groups. Consuming the investigated foods containing antioxidant phytochemicals may combat cardiac toxicity and oxidative stress. Nonetheless, thorough investigations and clinical monitoring are required to understand these functional foods' mechanism of action and dose-response effects in treating cardiotoxicity and oxidative stress.

Effect of Aronia melanocarpa fruit juice on glucose tolerance, lipid metabolism, and obesity in a rat model of metabolic syndrome

Abstract Metabolic syndrome (MS) is a serious health condition. The purpose of this study was to investigate the effects of polyphenol-rich Aronia melanocarpa fruit juice (AMFJ) on glucose tolerance, triglyceride levels, and adipose tissue in rats with MS induced by high-fat high-fructose (HFHF) diet. Fifty rats were allocated in 5 groups: control, MS, MS+AMFJ2.5, MS+AMFJ5, and MS+AMFJ10. In the course of 10 weeks, the control group was on a regular rat diet while the other groups received HFHF diet. During the experiment, control and MS groups were treated daily orally with distilled water (10.0 mL kg−1) and the other three groups – with AMFJ at doses of 2.5, 5.0, and 10.0 mL kg−1, respectively. In MS rats, glucose intolerance, hypertriglyceridemia, visceral obesity, and increased adipocyte size were observed. In AMFJ-treated groups, the serum glucose and triglycerides, as well as visceral fat and adipocyte size decreased significantly and did not differ from those of the control group. AMFJ at doses 2.5 and 5.0 mL kg−1 showed an anti-apoptotic activity in adipocytes, while at the dose of 10 mL kg−1 a pro-apoptotic effect was detected. In conclusion, AMFJ could antagonise most of the negative consequences of HFHF diet on carbohydrate and lipid metabolism in a rat MS model.

Effect of probiotic on mast cell density and expression of tryptase, chymase, and TNF-α in the urinary bladder of rats with high cholesterol

In this study, it was aimed to immunohistochemically evaluate the possible effect of probiotic supplementation on rats fed a high cholesterol diet on mast cell heterogeneity and density in the urinary bladder and on the expression of chymase, tryptase and tumor necrosis factor-alpha (TNF-α) cytokine in the urinary bladder. Three groups were formed in the study. For 8 weeks, Group 1 (control group) was fed regular rat diet. Food for Group 2 (feeding +2% cholesterol) (high cholestrol group) was provided for 8 weeks. For the last four weeks, Group 3 (%2 cholesterol + Lactobacillus acidophilus) (probiotic group) was administered L. acidophilus probiotics. Levels of total cholesterol (TC) was measured by using a spectrophotometric autoanalyzer. Serum TC levels were remarkably increased in group 2 compared to the group 1 (P&amp;lt;0.05). TC decreased significantly (P &amp;lt;0.05) in group 3 compared to group 2. The number of mast cells in the control group and the probiotic group were close to each other. Only safranin O (SO) (+) mast cells was increased in the probiotic group. While there was no difference between control and high cholesterol groups, an increase in the number of tryptase mast cells was found in the probiotic group. The number of chymase mast cells declined in the probiotic group compared to control and high cholesterol groups. There was no significant difference in TNF-α immunoreactivity between the three groups. In conclusion, in this study, possible effects of cholesterol and probiotics on mast cell heterogeneity and expression of chymase, tryptase, TNF-α were revealed.

Reversion to regular diet with alternate day fasting can cure grade-I non-alcoholic fatty liver disease (NAFLD) in high-fructose-intake-associated metabolic syndrome

BackgroundNon-alcoholic fatty liver disease (NAFLD) is an emerging global health problem that accompanied the obesity epidemic and is considered as the hepatic component of metabolic syndrome (MetS). Modification of lifestyle of MetS patients remains the focus to reverse and prevent progression of hepatic steatosis to NAFLD and its worsening to severe forms. The present study investigates the possible curability of metabolic syndrome -associated grade-1 NAFLD merely by alternate day fasting with or without reversion to regular diet in adult male rats. The present study was performed on 66 local strain male rats aged (6–10 m.) distributed randomly into C group (n = 12), on regular rat diet; and M group (n = 54) on high fructose- intake. On the 8th week, then rats were subjected to measurement of BW, BMI, WC, FBG, IPGTT, HDL-C, TGs, and liver histopathology, to include MetS rats randomly into four experimental groups for 4 weeks as follows: MS (n = 14); MSRD (n = 12); MSF (n = 13); and MSRDF (n = 12). On the 12th week, all rats were subjected to measurements of BW, BMI, WC, LW, LW/BW, VFW, VFW/BW, FBG, IPGTT, Ins., HOMA-IR, HbA1C, TGs, TC, LDL-C, HDL-C, CRP, Alb., bilirubin, ALT, L-MDA, and liver histopathology.ResultsOn the 8th week, M group developed MerS and grade-I NAFLD with score-4 hepatosteatosis (69%). On the 12th week, MS group had grade-1 NAFLD with score-4 hepatosteatosis (82%) with significantly increased Ins., HOMA-IR, HDL-C, LW, LW/BW, L-MDA, ALT, CRP, and significantly decreased Alb. than C rats. Both MSRD and MSF groups had grade-1 NAFLD with score-3 hepatosteatosis (42%) with significantly decreased Ins., HOMA-IR, TC, LDL-C, LW, LW/BW, L-MDA, ALT, CRP, and significantly increased HDL-C and Alb. than MS group. MSRDF rats showed cure of grade-1 NAFLD and significantly decreased LW than other groups and normalized HOMA-IR, HbA1C TC, LDL-C, ALT, and CRP.ConclusionOne month of alternate-day fasting and regular rat diet could cure grade-I NAFLD associated with Mets due to high fructose intake possibly by attenuating metabolic disorders. These two interventions might be recommended in the management of MetS patients with grade 1-NAFLD disease.

Tanshinone IIA ameliorates non-alcoholic fatty liver disease through targeting peroxisome proliferator-activated receptor gamma and toll-like receptor 4.

ObjectiveTo investigate the cellular mechanisms of action of tanshinone IIA on the fatty liver disease induced by a high-fat diet in an animal model of non-alcoholic fatty liver disease (NAFLD).MethodsAdult male Sprague Dawley rats were randomized into one of three groups: regular rat diet (CON group) for 4 months; high-fat diet (HFD group) for 4 months; HFD for 2 months followed by tanshinone IIA treatment plus HFD (TAN group) for a further 2 months. A range of physical and biochemical markers of lipid accumulation and fatty liver disease were measured and compared between the groups.ResultsTanshinone IIA treatment significantly reduced fat accumulation in the liver and plasma lipid levels that had been increased by HFD. The toll-like receptor (TLR4)/nuclear factor kappa B (NF-κB) signalling pathway was silenced by tanshinone IIA treatment. Tumour necrosis factor-α and interleukin-6 were reduced by tanshinone IIA. Hepatocyte apoptosis was inhibited by tanshinone IIA. Tanshinone IIA upregulated peroxisome proliferator-activated receptor gamma (PPAR-γ), which resulted in an improvement in the oxidative status.ConclusionTanshinone IIA ameliorates NAFLD by targeting PPAR-γ and TLR4, resulting in decreased plasma lipids and oxidative stress, suggesting this strategy may form the basis of novel NAFLD therapies.

Hydro-alcoholic Extract of Commiphora mukul Gum Resin May Improve Cognitive Impairments in Diabetic Rats

Background: Diabetes causes cognitive impairment. Medicinal plants due to different mechanisms, such as antioxidant activities may improve diabetes and relieve its symptoms. Commiphora mukul (Burseraceae) has a significant antioxidant activity. Objectives: This study aimed to examine the effect of hydro- alcoholic extract of C. mukul on passive-avoidance learning and memory in streptozotocin (STZ) induced diabetic male rats. Materials and Methods: Thirty-two adult male Wistar rats were randomly allocated to four groups: normal, diabetic, normal + extract of C. mukul and diabetic + extract of C. mukul groups with free access to regular rat diet. Diabetes was induced in male rats by single interaperitoneal injection of 60 mg/kg STZ. After the confirmation of diabetes, 300 mg/kg C. mukul extract was orally administered to the extract-treated groups. Control groups received normal saline at the same time. Passive-avoidance memory was tested eight weeks after the STZ treatment, and blood glucose and body weight were measured in all groups at the beginning and end of the experiment. Results: In the present study, diabetes decreased learning and memory. Although the administration of C. mukul extract did not affect the step-through latency (STLa) and the number of trials of the diabetic groups during the first acquisition trial, a significant decrease was observed in STLr and also a significant increase in time spent in the dark compartment (TDC) and number of crossing (NOC) in the retention test (after 24 and 48 hours). Although no significant difference was observed in body weight of diabetic + extract of C. mukul (DE) and diabetic control (DC) groups, the plasma glucose of DE group was significantly lower in comparison to DC group. Conclusions: Commiphora mukul extract can improve passive-avoidance learning and memory impairments in the STZ-induced diabetic rats. This improvement may be due to the antioxidant, acetylcholinesterase inhibitory activity, anti-inflammatory or power to reduce hyperglycemia and lowering cholesterol and triglyceride properties of this extract. The result of this study is a promising point for new therapeutic alternatives in alleviating cognitive impairments caused by diabetes.

The effect of butter oil on avoidance memory in normal and diabetic rats.

Since diabetes mellitus is accompanied by cognitive impairment in diabetic patient and animal models and since lipids play important roles in neuronal membrane composition, structure and function; we intended to evaluate the effect of dietary butter oil on passive avoidance memory of streptoztosin (STZ)-induced diabetic rats in this study. THIRTY SIX ADULT MALE RATS WERE RANDOMLY ALLOCATED TO FOUR EQUAL GROUPS: normal (N) and diabetic control (D) groups with free access to regular rat diet; but the diet of normal butter oil (NB) and diabetic butter oil (DB) groups was supplemented with 10% butter oil. Diabetes in D and DB groups was induced by intravenous (i.v.) injection of 50 mg/kg.bw of STZ. Passive avoidance memory and cholesterol of brain and hippocampal tissues has been measured six weeks after diabetes confirmation. Diabetes, especially in diabetic butter oil group decreased the abilities of learning and memory. The level of cholesterol in hippocampus was higher in NB (P< 0.05) and DB (P< 0.01) groups. We suggest consumption of butter oil may worsen cognitive impairment of diabetic animal. This may be related to the higher elevation of cholesterol in the hippocampus of diabetic animals.

Dietary fish oil prevents vascular dysfunction and oxidative stress in hyperinsulinemic rats

Fish oil has been shown to improve blood pressure (BP) in some disease states by an unknown mechanism. We tested the ability of fish oil to prevent vascular dysfunction in fructose-fed rats, a model of insulin resistance and hypertension. Rats were placed on three diets: 1) regular rat diet (control); 2) diet containing 60% fructose (FFR); or 3) diet containing 60% fructose and 4.4% fish oil (FFR+FO). After 8 weeks, blood, heart, aorta, and mesenteric artery tissue were collected from each animal. Secondary branch segments of mesenteric arteries were isolated for vascular reactivity studies. Systolic BP increased significantly in the FFR but was reduced to control levels by the addition of fish oil to the diet. In the mesenteric artery segments from FFR, the dose-response curves to acetylcholine were significantly shifted to the right compared with those of control rats and rats on the fish oil diet. Expression of endothelial nitric oxide synthase (eNOS) protein and mRNA was reduced in the FFR aortas and hearts, and this reduction was reversed by the fish oil. Dietary fish oil prevented the hyperlipidemia that occurred in the FFR but did not prevent hyperinsulinemia. Plasma concentrations of hydrogen peroxide, 8-isoprostane, and monocyte chemoattractant protein-1 were significantly elevated in the FFR and were significantly lower in the FFR treated with fish oil. These results demonstrate that dietary fish oil prevents vascular dysfunction in FFR and that this effect of fish oil is associated with increased eNOS expression and decreased oxidative stress.

Detrimental effects of the ketogenic diet on cognitive function in rats.

The ketogenic diet (KD) is a high-fat, low-carbohydrate, and low-protein diet that is widely used to treat epilepsy in children. Although the KD has been shown to be efficacious in the treatment of childhood epilepsy, the long-term effects of the KD on brain development are not clear. The objective of this study was to examine the long-term effects of the KD on visual-spatial memory, activity level, and emotionality in immature rats after status epilepticus (SE). Weanling rats were subjected to lithium/pilocarpine-induced SE or saline injections and were then randomized to either the KD or regular rat diet, both fed ad libitum. One month later, rats were evaluated for visual-spatial memory in the water maze, activity level in the open field test, and emotionality with the handling test. Spontaneous recurrent seizures were measured using videotaping, and seizure susceptibility was tested with flurothyl inhalation. Brains were weighed and examined for mossy fiber sprouting and cell loss. Although rats treated with the KD were active and seemed healthy, their weight gain was substantially lower than that in rats that received regular rat diet. The KD reduced the number of spontaneous seizures but had no discernible effect on flurothyl seizure susceptibility. KD-fed rats, with or without SE, had significantly impaired visual-spatial learning and memory compared with rats that were fed regular diet. The KD had minimal effects on activity level and emotionality. Rats that were treated with the KD had significantly impaired brain growth. No differences in pathology scores between the KD and regular diet groups were seen after SE. Despite reducing the number of spontaneous seizures after SE, the KD resulted in severe impairment in visual-spatial memory and decreased brain growth, with no effect on mossy fiber sprouting. This study raises concerns about the long-term effects of the KD on brain development.

Central leptin gene therapy blocks high-fat diet-induced weight gain, hyperleptinemia, and hyperinsulinemia: increase in serum ghrelin levels.

Recombinant adeno-associated virus (rAAV), encoding either rat leptin (rAAV-lep) or green fluorescent protein (rAAV-GFP, control), was injected intracerebroventricularly in rats consuming a high-fat diet (HFD; 45 kcal%). Caloric consumption and body weight were monitored weekly until the rats were killed at 9 weeks. Untreated control rats consuming regular rat diet (RCD; 11 kcal%) were monitored in parallel. Body weight gain was accelerated in rAAV-GFP + HFD control rats relative to those consuming RCD, despite equivalent kcal consumption. At 9 weeks, serum leptin, free fatty acids, triglycerides, and insulin were elevated in HFD control rats. In contrast, rAAV-lep treatment reduced intake and blocked the HFD-induced increase in weight, adiposity, and metabolic variables. Blood glucose was slightly reduced but within the normal range, and serum ghrelin levels were significantly elevated in rAAV-lep + HFD rats. Uncoupling protein-1 (UCP1) mRNA in brown adipose tissue (BAT), an index of energy expenditure through nonshivering thermogenesis, was decreased in rats consuming HFD. Treatment with rAAV-lep significantly augmented BAT UCP1 mRNA expression, indicating increased thermogenic energy expenditure. These findings demonstrate that central leptin gene therapy efficiently prevents weight gain, increased adiposity, and hyperinsulinemia in rats consuming an HFD by decreasing energy intake and increasing thermogenic energy expenditure.

Anti-neutrophil serum attenuates dextran sulfate sodium-induced colonic damage in the rat.

The role of neutrophils in experimental colonic damage induced by dextran sulfate sodium is uncertain. We test the hypothesis that neutrophils are of pathogenic significance and anti-neutrophil serum will attenuate the colonic damage induced by oral dextran sulfate sodium in rats. Rabbit anti-rat neutrophil serum (anti-neutrophil serum) or control rabbit serum was administered to, and circulating neutrophil count was monitored in, rats before and during feeding of dextran sulfate sodium or regular rat diet for 2 weeks. Histologic features of mucosal damage were evaluated in hematoxylin and eosin-stained proximal and distal colonic sections by a blinded observer. Oral dextran sulfate sodium induces weight loss, diarrhea, peripheral neutrophilia, and colonic damage. Anti-neutrophil serum induced neutropenia and significantly attenuated the weight loss, the neutrophil infiltration in the colon, and the mucosal necrosis and pathologic index in the distal colon. The data showing that anti-neutrophil serum attenuates distal colonic mucosal injury induced by dextran sulfate sodium support the hypothesis that neutrophils play a pathogenic role in this model of colonic mucosal damage.

Hemodynamic and metabolic effects of hypomagnesemia in spontaneously hypertensive rats.

The hemodynamic and metabolic effects of dietary induced hypomagnesemia were studied in two groups of 2-month-old male spontaneously hypertensive rats (SHR). All rats were given distilled water to drink ad libitum and were followed for 2 months. However, control rats (n = 12) were given a regular rat diet to eat, whereas the experimental (hypomagnesemic; HM) rats (n = 12) were given a magnesium-free diet. Metabolic and hemodynamic studies were done at the end of the 2-month observation period in the awake state. HM rats had higher mean arterial pressure, total peripheral resistance, renal vascular resistance, heart rate, UNaV, UKV and serum Na, and lower hematocrit, renal blood flow, serum K and serum Mg than the controls. No differences were observed among the two groups of rats with respect to weight, fluid intake, urine volume, serum calcium, blood urea nitrogen, cardiac index and glomerular filtration rate. In addition, HM rats had widespread myocardial and renal tissue calcification in contrast to controls, which did not show any tissue calcification. We conclude: (1) dietary-induced hypomagnesemia aggravated the hypertension of SHR; (2) it caused widespread tissue calcification; (3) the adverse effects of hypomagnesemia on arterial pressure were possibly produced through calcium-mediated systemic vasoconstriction and increase in peripheral vascular resistance.

CHOLINERGIC INFLUENCES ON HYPOTHALAMIC-PITUITARY-ADRENOCORTICAL ACTIVITY OF STRESSED RATS: AN APPROACH UTILIZING CHOLINE DEFICIENT DIETS

Male rats were placed on choline (Ch) deficient diets for 3 to 14 days, without and with Ch (normal and large doses) supplemented in the drinking water, to determine whether altering the availability of Ch would affect the cholinergic system in relation to the latter's role in modulating the hypothalamic-pituitary-adrenocortical (HPA) system of non-stressed and stressed animals. The results indicate that the basal nonstressed activity of the HPA system, as assessed by adrenal and plasma corticosterone concentrations, was not affected by placing the animals on these diets for as long as 14 days. Furthermore, the in vitro production of corticosterone by these adrenal glands, in the presence or absence of adrenocorticotrophin, was similar to those observed in animals on the regular rat diet; however, the HPA responses to auditory (100 db) stress, and to a lesser extent hypercapnic (9% CO2) stress, were impaired on the Ch deficient diet (14 days), and these responses were partially corrected by supplementing the diet with Ch in the drinking water. Thus, the data suggest that altering the dietary intake of Ch may affect cholinergic activity, which in turn affects the HPA response to stressors.