scholarly journals Age-specific and Dose-dependent Retinal Dysplasia and Degeneration Induced by a Single Intraperitoneal Administration of N-Methyl-N-nitrosourea to Rats.

1998 ◽  
Vol 11 (2) ◽  
pp. 127-131 ◽  
Author(s):  
Hiroyuki Nambu ◽  
Katsuhiko Yoshizawa ◽  
Jihong Yang ◽  
Daigo Yamamoto ◽  
Airo Tsubura
Keyword(s):  
Intraperitoneal Administration ◽  
Retinal Dysplasia ◽  
Dose Dependent

Evaluation of Hepatoprotective activity of Methanol extract of Persicaria hydropiper: An in vivo screening

2021 ◽  
pp. 5819-5824
Author(s):  
Pooja Kamra ◽  
Mahaveer Singh ◽  
Hardarshan Singh Lamba ◽  
Birendra Srivastava
Keyword(s):  
Carbon Tetrachloride ◽  
Intraperitoneal Administration ◽  
Hepatoprotective Activity ◽  
Dependent Manner ◽  
Standard Drug ◽  
Whole Plant ◽  
Dose Dependent ◽  
Histopathological Investigation ◽  
Different Doses

The present study aimed to evaluate the hepatoprotective potential of methanolic whole plant extract of Persicaria hydropiper in carbon tetrachloride (CCl4) induced hepatotoxicity model. Hepatotoxicity was induced in rats by intraperitoneal administration of carbon tetrachloride (CCl4) for seven days. The extract was thereafter administered at two different doses of 200 mg/kg and 400 mg/kg body weight for next seven days. Silymarin was used as a reference standard. The extract revealed hepatoprotective activity in dose dependent manner. The dose of 400 mg/kg exhibited maximum hepatoprotective ability as apparent from several evaluation parameters including liver function profile, bilirubin, antioxidant enzymes as well as histopathological investigation which was comparable to the standard drug Silymarin respectively. These findings sustenance the use of the extract as an adjuvant with existing therapy for treatment of liver ailments.

Effects of central and systemic administration of leptin on neurotransmitter concentrations in specific areas of the hypothalamus

2006 ◽  
Vol 290 (2) ◽  
pp. R306-R312 ◽  
Author(s):  
Kimberly A. Clark ◽  
Sheba M. J. MohanKumar ◽  
Badrinarayanan S. Kasturi ◽  
P. S. MohanKumar
Keyword(s):  
Intraperitoneal Administration ◽  
Ventromedial Hypothalamus ◽  
Systemic Administration ◽  
Male Rats ◽  
Dependent Manner ◽  
Intracerebroventricular Administration ◽  
Dorsal Nucleus ◽  
Intracerebroventricular Injections ◽  
Dose Dependent ◽  
Pituitary Adrenal Axis

Leptin, a hormone produced by adipocytes, has been shown to affect a number of central functions, such as regulation of the hypothalamo-pituitary-adrenal axis, feeding, and body weight regulation. Because hypothalamic monoamines are intricately involved in the regulation of these functions, we hypothesized that leptin may produce its effects by altering the activity of these neurotransmitters. To test this hypothesis, male rats received peripheral (0, 100, or 500 μg ip), or central (0 or 5 μg icv) injections of leptin. The animals were killed 5 h later, and their brains were removed, frozen, and sectioned. Serum was collected to measure leptin and corticosterone by RIA. The paraventricular nucleus (PVN), arcuate nucleus (AN), ventromedial hypothalamus (VMH), dorsomedial dorsal nucleus (DMD), median eminence (ME), and medial preoptic area (MPA) were obtained using Palkovits' microdissection technique, and monoamine concentrations in these areas were determined using HPLC-EC. Intraperitoneal administration of leptin increased serum leptin concentrations in a dose-dependent manner ( P < 0.05). Both intraperitoneal and intracerebroventricular administration of leptin decreased serum corticosterone significantly ( P < 0.05). Norepinephrine (NE) concentration decreased significantly in the PVN, AN, and VMH after both intraperitoneal and intracerebroventricular administration of leptin ( P < 0.05). NE concentrations decreased significantly in the DMN after intracerebroventricular administration of leptin ( P < 0.05). Leptin treatment (both ip and icv) decreased dopamine concentrations significantly in the PVN. Serotonin (5-HT) concentration decreased significantly in the PVN after both intraperitoneal and intracerebroventricular injections of leptin and decreased in the VMH only with intracerebroventricular treatment of leptin. Leptin did not affect any of the monoamines in the ME and MPA. These results indicate that both central and systemic administration of leptin can affect hypothalamic monoamines in a region-specific manner, which, in turn, could mediate many of leptin's central and neuroendocrine effects.

scholarly journals The Immunomodulatory Effects of AlbuminIn VitroandIn Vivo

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Derek S. Wheeler ◽  
John S. Giuliano ◽  
Patrick M. Lahni ◽  
Alvin Denenberg ◽  
Hector R. Wong ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lethal Dose ◽  
Intraperitoneal Administration ◽  
Peritoneal Macrophages ◽  
Luciferase Reporter Assay ◽  
Luciferase Reporter ◽  
Reporter Assay ◽  
Dose Dependent

Albumin appears to have proinflammatory effectsin vitro. We hypothesized that albumin would induce a state of tolerance to subsequent administration of lipopolysaccharide (LPS)in vitroandin vivo. RAW264.7 and primary peritoneal macrophages were treated with increasing doses of bovine serum albumin (BSA) and harvested for NF-κB luciferase reporter assay or TNF-αELISA. In separate experiments, RAW264.7 cells were preconditioned with 1 mg/mL BSA for 18 h prior to LPS (10 μg/mL) treatment and harvested for NF-κB luciferase reporter assay or TNF-αELISA. Finally, C57Bl/6 mice were preconditioned with albumin via intraperitoneal administration 18 h prior to a lethal dose of LPS (60 mg/kg body wt). Blood was collected at 6 h after LPS administration for TNF-αELISA. Albumin produced a dose-dependent and TLR-4-dependent increase in NF-κB activation and TNF-αgene expressionin vitro. Albumin preconditioning abrogated the LPS-mediated increase in NF-κB activation and TNF-αgene expressionin vitroandin vivo. The clinical significance of these findings remains to be elucidated.

scholarly journals Phenyl N -tert-butylnitrone, a Free Radical Scavenger, Reduces Mechanical Allodynia in Chemotherapy-induced Neuropathic Pain in Rats

2010 ◽  
Vol 112 (2) ◽  
pp. 432-439 ◽  
Author(s):  
Hee Kee Kim ◽  
Yan Ping Zhang ◽  
Young Seob Gwak ◽  
Salahadin Abdi
Keyword(s):  
Neuropathic Pain ◽  
Free Radical ◽  
Mechanical Allodynia ◽  
Intraperitoneal Administration ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Dependent Manner ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Dose Dependent

Background Paclitaxel is a widely used chemotherapeutic drug for breast and ovarian cancer. Unfortunately, it induces neuropathic pain, which is a dose-limiting side effect. Free radicals have been implicated in many neurodegenerative diseases. The current study tests the hypothesis that a free radical scavenger plays an important role in reducing chemotherapy-induced neuropathic pain. Methods Neuropathic pain was induced by intraperitoneal injection of paclitaxel (2 mg/kg) on four alternate days (days 0, 2, 4, and 6) in male Sprague-Dawley rats. Phenyl N-tert-butylnitrone (PBN), a free radical scavenger, was administered intraperitoneally as a single dose or multiple doses before or after injury. Mechanical allodynia was measured by using von Frey filaments. Results The administration of paclitaxel induced mechanical allodynia, which began to manifest on days 7-10, peaked within 2 weeks, and plateaued for at least 2 months after the first paclitaxel injection. A single injection or multiple intraperitoneal injections of PBN ameliorated paclitaxel-induced pain behaviors in a dose-dependent manner. Further, multiple administrations of PBN starting on day 7 through day 15 after the first injection of paclitaxel completely prevented the development of mechanical allodynia. However, an intraperitoneal administration of pbn for 8 days starting with the first paclitaxel injection did not prevent the development of pain behavior. Conclusions This study clearly shows that PBN alleviated mechanical allodynia induced by paclitaxel in rats. Furthermore, our data show that PBN given on days 7 through 15 after the first paclitaxel injection prevented the development of chemotherapy-induced neuropathic pain. This clearly has a clinical implication.

scholarly journals Effects of Orally Consumed Rosa damascena Mill. Hydrosol on Hematology, Clinical Chemistry, Lens Enzymatic Activity, and Lens Pathology in Streptozotocin-Induced Diabetic Rats

Molecules ◽  
2019 ◽  
Vol 24 (22) ◽  
pp. 4069
Author(s):  
İlker Demirbolat ◽  
Cansu Ekinci ◽  
Fadime Nuhoğlu ◽  
Murat Kartal ◽  
Pelin Yıldız ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Enzymatic Activity ◽  
Aldose Reductase ◽  
Clinical Chemistry ◽  
Intraperitoneal Administration ◽  
Diabetic Rats ◽  
Rosa Damascena ◽  
Dependent Manner ◽  
Chronic Hyperglycemia ◽  
Dose Dependent

Diabetes mellitus is a multisystemic metabolic disorder that may affect the eyes, kidneys, vessels, and heart. Chronic hyperglycemia causes non-enzymatic glycation of proteins and elevation of the polyol pathway resulting in oxidative stress that damages organs. The current study aimed to investigate the dose-dependent effects of orally consumed Rosa damascena Mill. hydrosol on hematology, clinical biochemistry, lens enzymatic activity, and lens pathology in streptozotocin (STZ)-induced diabetic rats. Diabetes was induced into male Sprague–Dawley rats by intraperitoneal administration of STZ (40 mg/kg body weight). Rose hydrosols containing 1515 mg/L and 500 mg/L total volatiles (expressed as citronellol) were introduced to rats orally for 45 days. Consumption of 1515 mg/L volatile containing rose hydrosol successfully ameliorated hematologic, hepatic, and renal functions. Hydrosols also attenuated hyperglycemia and decreased the advanced glycation end-product formation in a dose-dependent manner. Rose hydrosol components significantly increased the lens enzymatic activities of glutathione peroxidase and decreased the activity of aldose reductase to prevent cataractogenesis. Histopathological examinations of rat lenses also indicated that increasing the dose of rose hydrosol had a protective effect on lenses in diabetic conditions. Additionally, in silico modeling of aldose reductase inhibition with rose hydrosol volatiles was carried out for extrapolating the current study to humans. The present results suggest that rose hydrosol exerts significant protective properties in diabetes mellitus and has no toxic effect on all studied systems in healthy test groups.

scholarly journals Effects of acute ethanol administration on rat liver 5-aminolaevulinate synthase activity

1989 ◽  
Vol 262 (2) ◽  
pp. 491-496 ◽  
Author(s):  
A A B Badawy ◽  
C J Morgan ◽  
N R Davis
Keyword(s):  
Alcohol Dehydrogenase ◽  
Rat Liver ◽  
Intraperitoneal Administration ◽  
Reciprocal Relationship ◽  
Ethanol Administration ◽  
Simultaneous Increase ◽  
Acute Ethanol ◽  
Tryptophan Pyrrolase ◽  
Dose Dependent Decrease ◽  
Dose Dependent

1. Liver 5-aminolaevulinate (ALA) synthase activity of 24 h-starved rats is maximally increased at 4 h after intraperitoneal administration of a 1.6 g/kg body wt. dose of ethanol. Larger doses cause a dose-dependent decrease in the extent of this stimulation, exhibiting a reciprocal relationship with an elevation of hepatic haem concentration, as suggested by the simultaneous increase in the haem saturation of tryptophan pyrrolase. 2. ALA synthase induction by ethanol is abolished if the above increase in pyrrolase saturation with haem is enhanced by theophylline, but is potentiated when the increase in the haem saturation is inhibited by anti-lipolytic agents. 3. ALA synthase induction by ethanol is also inhibited by inhibitors of alcohol dehydrogenase and aldehyde dehydrogenase. Acetaldehyde and acetate are, however, not responsible; they both decrease ALA synthase activity and increase the haem saturation of tryptophan pyrrolase. These latter effects of acetaldehyde are not mediated by acetate. 4. ALA synthase activity is also stimulated by succinate, which, however, also increases the haem saturation of tryptophan pyrrolase. 5. Ethanol does not influence the rate of ALA synthase degradation. 6. It is suggested that ethanol increases rat liver ALA synthase activity as a result of its own metabolism by the alcohol dehydrogenase-dependent pathway by a mechanism not involving decreased degradation of the former enzyme or the participation of the metabolites acetaldehyde and acetate.

Role of cytochrome P-450 in endogenous antipyresis

2000 ◽  
Vol 279 (2) ◽  
pp. R455-R460 ◽  
Author(s):  
Wieslaw Kozak ◽  
Matthew J. Kluger ◽  
Anna Kozak ◽  
Maciej Wachulec ◽  
Karol Dokladny
Keyword(s):  
Arachidonic Acid ◽  
Intraperitoneal Administration ◽  
Dependent Manner ◽  
Epoxyeicosatrienoic Acid ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Rats And Mice ◽  
Dose Dependent ◽  
Cytochrome P 450

In previous reports, we (15, 18) and others (29) demonstrated data showing that various inhibitors of cytochrome P-450/epoxygenase augment fever in rats and mice, indicating that the enzyme may be involved in endogenous antipyresis. The aim of this study was to further test the hypothesis that the P-450-dependent epoxygenase pathway of arachidonic acid is part of the homeostatic system to control the height of fever. Sprague-Dawley rats were implanted with biotelemeters to monitor body temperature. Fever was induced by intraperitoneal injection of lipopolysaccharide (LPS; 80 μg/kg). We demonstrate that intraperitoneal administration of P-450 inducers (bezafibrate and dehydroepiandrosterone, 10 and 100 mg/kg) before LPS reduced fever in rats in a dose-dependent manner. In complementary experiments, rats were implanted with brain cannulas in addition to the biotelemeters. Various isomers of epoxyeicosanoids were administered into the lateral ventricle at doses of 0.01 to 10 μg/rat to test their influence on LPS-induced fever in rats. Four of five isomers were antipyretic in a dose-dependent manner. The most potent antipyretic isomers were 11,12-epoxyeicosatrienoic acid (EET) followed by 14,15-EET, 8,9-EET, and 12(R) hydroxyeicosatetraenoic acid. These data support the hypothesis that the cytochrome P-450/epoxygenase pathway of arachidonate metabolism is part of the endogenous antipyretic system.

scholarly journals Pharmacological stimulation of brain carnitine palmitoyl-transferase-1 decreases food intake and body weight

2008 ◽  
Vol 294 (2) ◽  
pp. R352-R361 ◽  
Author(s):  
Susan Aja ◽  
Leslie E. Landree ◽  
Amy M. Kleman ◽  
Susan M. Medghalchi ◽  
Aravinda Vadlamudi ◽  
...  
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Fatty Acid ◽  
Food Intake ◽  
Taste Aversion ◽  
Conditioned Taste Aversion ◽  
Fatty Acid Synthase ◽  
Intraperitoneal Administration ◽  
Carnitine Palmitoyl Transferase ◽  
Dose Dependent

Inhibition of brain carnitine palmitoyl-transferase-1 (CPT-1) is reported to decrease food intake and body weight in rats. Yet, the fatty acid synthase (FAS) inhibitor and CPT-1 stimulator C75 produces hypophagia and weight loss when given to rodents intracerebroventricularly (icv). Thus roles and relative contributions of altered brain CPT-1 activity and fatty acid oxidation in these phenomena remain unclarified. We administered compounds that target FAS or CPT-1 to mice by single icv bolus and examined acute and prolonged effects on feeding and body weight. C75 decreased food intake rapidly and potently at all doses (1–56 nmol) and dose dependently inhibited intake on day 1. Dose-dependent weight loss on day 1 persisted through 4 days of postinjection monitoring. The FAS inhibitor cerulenin produced dose-dependent (560 nmol) hypophagia for 1 day, weight loss for 2 days, and weight regain to vehicle control by day 3. The CPT-1 inhibitor etomoxir (32, 320 nmol) did not alter overall day 1 feeding. However, etomoxir attenuated the hypophagia produced by C75, indicating that CPT-1 stimulation is important for C75's effect. A novel compound, C89b, was characterized in vitro as a selective stimulator of CPT-1 that does not affect fatty acid synthesis. C89b (100, 320 nmol) decreased feeding in mice for 3 days and produced persistent weight loss for 6 days without producing conditioned taste aversion. Similarly, intraperitoneal administration decreased feeding and body weight without producing conditioned taste aversion. These results suggest a role for brain CPT-1 in the regulation of energy balance and implicate CPT-1 stimulation as a pharmacological approach to weight loss.

Characterization of the Effects of Gabapentin and 3-Isobutyl-γ-Aminobutyric Acid on Substance P-induced Thermal Hyperalgesia 

1998 ◽  
Vol 88 (1) ◽  
pp. 196-205 ◽  
Author(s):  
Brett J. Partridge ◽  
Sandra R. Chaplan ◽  
Eiji Sakamoto ◽  
Tony L. Yaksh
Keyword(s):  
Substance P ◽  
Intrathecal Injection ◽  
Intraperitoneal Administration ◽  
Thermal Hyperalgesia ◽  
Radiant Heat ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Plantar Surface ◽  
Withdrawal Latency ◽  
Dose Dependent

Background The authors sought to characterize the pharmacologic characteristic and site of action of gabapentin (Neurontin) in a model of thermal hyperalgesia induced by intrathecal substance P administration. Methods Rats were prepared with long-term lumbar intrathecal catheters. Hind paw withdrawal latency was determined using a radiant heat stimulus focused through a glass surface onto the plantar surface of the paw. Results Within 5 min after intrathecal injection of substance P (30 nmol), hind paw withdrawal latency fell from 11 to 8 s. Gabapentin given intrathecally or intraperitoneally produced dose-dependent reversal of the thermal hyperalgesia, with complete reversal (ED100) occurring at 163 microg for intrathecal and 185 mg/kg for intraperitoneal administration. S(+)-3-isobutyl-gamma aminobutyric acid, but not R(-)-3-isobutyl-gamma aminobutyric acid, also produced dose-dependent reversal of the intrathecal substance P-induced thermal hyperalgesia (intrathecal ED100, 65 microg and intraperitonal ED100, 31 mg/kg). The effects of intraperitoneally administered gabapentin and 3-isobutyl-gamma aminobutyric acid were reversed by intrathecal pretreatment with D-serine (100 microg) but not by L-serine. All effects were observed at doses that had little effect on motor function or spontaneous activity. Intrathecal N-methyl-D-aspartate (2 nmol) induced thermal hyperalgesia, which was blocked by gabapentin (100 mg/kg intraperitoneally) and S(+)-3-isobutyl-gamma aminobutyric acid (30 mg/kg intraperitoneally). Conclusions The structure-activity relationship and the stereospecificity noted after intrathecal delivery suggest that gabapentin and S(+)-3-isobutyl-gamma aminobutyric acid act at a common spinal locus to modulate selectively a facilitated state of nociceptive processing.

scholarly journals Antiabsence Effects of Safranal in Acute Experimental Seizure Models: EEG and Autoradiography

2008 ◽  
Vol 11 (3) ◽  
pp. 1 ◽  
Author(s):  
Hamid Sadeghnia ◽  
Miguel Cortez ◽  
Dick Liu ◽  
Hossein Hosseinzadeh ◽  
O. Carter Snead
Keyword(s):  
Binding Site ◽  
Gabaa Receptor ◽  
Mouse Brain ◽  
Gabab Receptor ◽  
Intraperitoneal Administration ◽  
Brain Regions ◽  
Crocus Sativus ◽  
Absence Seizures ◽  
Seizure Models ◽  
Dose Dependent

PURPOSE: We examined the effect of safranal, a constituent of Crocus sativus, in acute experimental animal models of generalized absence seizures. METHODS: We further characterized its effects on the GABAergic system through the regional modification of [3H] flunitrazepam, a benzodiazepine agonist binding site and [3H] CGP54626A, a GABAB receptor antagonist binding site in mouse brain. RESULTS: The systemic administration of safranal resulted in a significant and dose-dependent attenuation in experimental absence seizures elicited by either ?-butyrolactone (GBL), baclofen (BAC) or low doses of GABAA receptor antagonists; pentylenetetrazole (PTZ), picrotoxin (PTX) and bicuculline (BMC). After a single intraperitoneal administration of safranal (291 mg/kg), no changes in baseline electrocorticographic (ECoG) recording were observed, however, a significant decrease in [3H] flunitrazepam binding was seen in the cortex (33.16%, p<0.001), hippocampus (27.36%, p<0.01) and thalamus (29.91%, p<0.01) of mouse brain, while the [3H] CGP54626A binding did not show any modification in the same brain regions. CONCLUSION: These data indicate that there is an antiabsence seizure property in safranal and its effect may be due to modifications on the benzodiazepine binding sites of the GABAA receptor complex.

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