Objective: To three-dimensionally elucidate the effects of occlusal hypofunction on the periodontal ligament and alveolar bone proper of rat molars by micro-computed tomography (micro-CT). Methods: Occlusal function in the molar area was restricted by attaching an anterior bite plate on the maxillary incisors and a metal cap on the mandibular incisors of 5-week-old male Wistar rats for 1 week. The periodontal ligament space and alveolar bone proper around roots of the mandibular first molar were assessed by histology and micro-CT. Results: The periodontal ligament space was narrower and the alveolar bone proper was sparser and less continuous in the hypofunction group than in the control group. Further, both the volume of the periodontal ligament and the volumetric ratio of the alveolar bone proper to the total tissue in the region of interest were significantly lower in the hypofunction group (p < 0.05). Conclusions: Occlusal hypofunction induces atrophic changes in the periodontal ligament and alveolar bone proper of rat molars.
A glutathione peroxidase from white rat (Wistar strain)erythrocytes was partially purified and characterized. In addition, localization of this enzyme in the liver was studied by histochemical method. A glutathione peroxidase was purified approximately 33.5-folds by ammonium sulfate precipitation, Sephadex filtration column and DEAE-Sephadex column chromatography. The optimum temperature of the crude glutathione peroxidase was $40^\\circC$, and the optimum pH was 7.5. This crude glutathione peroxidase was most stable at $30^\\circC$ and the values of Km and Vmax were calculated to be 8.5mM and 15.6 $\\mu$moles/min for glutathione, and 40 $\\mu$M and 10.5 $\\mu$moles/min for hydrogen peroxide, respectively. The molecular weight of this enzyme was estimated by Sephadex G-200 gel filtration to be approximately 90, 000. By electron microscopic examination, histochemical reaction products were microbodies that were prominent in the peripheral parts of the lobule. The reaction products exhibited round shapes, the diameter of which varied $0.2\\sim0.7 \\muM$ and their boundary membranes were not distint.
Proceedings of the Korean Society of Applied Pharmacology
/
1994.04a
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pp.335-335
/
1994
Possibility whether lead ingestion can cause selective toxicity to central serotonergic nervous system in rats was tested. Three groups of wistar rats; 1)Control, 2) Low dose and 3) High dose groups, were prepared. In prenatally lead-exposed rats, until parturition from dams, rat pups were intoxicated via placenta of mother rats having received drinking water containing either 0%(control ), 0.05%(low dose) or 0.2%(high dose) of lead acetate respectively, In postnatally lead-exposed rats, right after parturition from dams rat pups received drinking water containing either 0% (control), 0.05%(low dose) or 0.2%(high dose) of lead acetate. At 2, 4, 6 and 8 weeks of age, tryptophan hydroxylase (TPH) activity and Na$\^$+//K$\^$+/-ATPase activity were measured in 4 areas of rat brain; Telencephalon, Diencephalon, Midbrain and Pons/Medulla. TPH activities were assayed by modified method of Beevers et al. (1983) using L-(5-$^3$H)-tryptophan as substrate. TPH activity was determined as a criterion of lead poisoning to central serotonergic nervous system and Na$\^$+//K$\^$+/-ATPase activity as a criterion of non specific lead poisoning to any kinds of tissues. Selective toxicity of lead poisoning to central serotonergic nervous system was evaluated by the changes of TPH activities without concomitant changes of Na$\^$+//K$\^$+/-ATPase activities. In prenatally lead-exposed rats. this selectivity was found in Telencephalon (2 weeks of age), Diencephalon/Midbrain (2 weeks of age), Midbrain (4 and 6 weeks of age), Pons/Medulla (2, 4 and 6 weeks of age) In rats exposed to low dose of lead and Pons/Medulla (2 weeks of age) to high dose of lead. In postnatal Iy lead-exposed rats, this selectivity was found in Telencephalon (8 weeks of age), Diencephalon(8 weeks of age), Pons/Medulla (6 and 8 weeks of age) in rats exposed to low dose of lead and Pons/Medulla (8 weeks of age) to high dose of lead. These results suggest that lead poisoning may exhibit selective toxicity to central serotonergic nervous system.
Jin, Eun-Sun;Kim, Ji Yeon;Lee, Bora;Min, JoongKee;Jeon, Sang Ryong;Choi, Kyoung Hyo;Jeong, Je Hoon
Journal of Korean Neurosurgical Society
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v.61
no.5
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pp.559-567
/
2018
Objective : The aim of this study was to evaluate the effect for biodegradable screws containing bone morphogenetic protein-2 (BMP-2) in an osteoporotic rat model. Methods : Twenty-four female Wistar rat (250-300 g, 12 weeks of age) were randomized into four groups. Three groups underwent bilateral ovariectomy (OVX). Biodegradable screws with or without BMP-2 were inserted in the proximal tibia in two implantation groups. The extracted proximal metaphysis of the tibiae were scanned by exo-vivo micro-computed tomography. Evaluated parameters included bone mineral density (BMD), trabecular bone volume (BV/TV), trabecular number, trabecular thickness, and trabecular separation (Tb.Sp). The tibia samples were pathologically evaluated by staining with by Hematoxylin and Eosin, and trichrome. Results : Trabecular formation near screw insertion site was evident only in rats receiving BMP-2 screws. BMD and BV/TV significantly differed between controls and the OVX and OVX with screw groups. However, there were no significant differences between control and OVX with screw BMP groups. Tb.Sp significantly differed between control and OVX and OVX with screw groups (p<0.05), and between the OVX and OVX with screw BMP group (p<0.05), with no statistically significant difference between control and OVX with screw BMP groups. Over the 12 weeks after surgery, bone lamellae in direct contact with the screw developed more extensive and thicker trabecular bone around the implant in the OVX with screw BMP group compared to the OVX with screw group. Conclusion : Biodegradable screws containing BMP-2 improve nearby bone conditions and enhance ostoeintegration between the implant and the osteoporotic bone.
Temporary clamping of the portal triad is a common strategy to minimize bleeding during liver transplantation. Increasing evidences suggests that oxygen derived free radicals and reintroduction of oxygen in ischemic tissue lead to ischemic and reperfusion injury (I/R) and lead to apoptosis and necrosis. Adult Wistar rat subjected to 60 min of partial liver ischemia followed by three hour reperfusion. Eighteen Wister rats were divided into sham-operated control group (I) (n = 6), ischemia and reperfusion group (II) (n = 6), folic acid treated group (1 mg/kg body weight/daily by oral route for 7 days before induced ischemia reperfusion maneuver) (III) (n = 6). Apoptotic and necrotic hepatocytes, mitochondrial antioxidant enzymes were measured. Liver injury was assessed by alanine transaminases (ALT), aspartate transaminases (AST), liver histopathology and electron microscopy. An ischemic and reperfusion hepatocellular injury was indicated by increased serum-ALT, AST, histopathology and electron microscopy studies. Apoptotic and necrotic cells were increased which was revealed by flow cytometry in I/R group. Pre- treatment with folic acid significantly decreased serum -ALT, AST levels, apoptotic and necrotic cells after 1 h ischemia followed by 3 h of reperfusion. Histopathology and TEM studies showed markedly diminished hepatocellular injury in folic acid pretreated rats during the hepatic I/R, which reached a level comparable to saline-treated rat of sham operated group. On the basis of our findings it may be concluded that folic acid afforded significant protection from necrosis and apoptosis in I/R injury.
Sildenafil citrate (SIL) a phosphodiesterase 5 inhibitor (PDE5I) has been used for long time as a first line oral drug for erectile dysfunction. Though it has beneficial effects on erectile organ it also has some adverse effects in other cells and/or tissues related to reproductive system when exposed to longer duration. The objective of the present study is to evaluate the long term effect of SIL on sperm parameters in Wistar albino rat. The animals are divided into two groups, for group I - rats were treated with saline (vehicle alone) and group - II oral administration of 5 mg/kg b.w. of SIL was administrated orally once in a day for 120 days. At the end of the trial period animals were sacrificed and epididymal sperm were subjected to various analysis. Results showed significant reduction in sperm count, motility, viability and morphologically intact sperm in long term PDE5I exposed animals when compared to control. Acrosomal status and fertility test also showed significant reduction in long term PDE5I exposed animals. The present study clearly indicated that long term SIL has shown to induce alteration in sperm quality and quantity, leading to decline in fertility rate. Indicate that SIL impinge on spermatogenesis as well as epididymal function. Understanding the molecular down-stream events involved in long-term exposure to PDE5 inhibitor can be valuable to supervise on related infertility issues and to suggest corrective measures.
This study was desinged to investigate the effect of estrogen(Est) on the proliferating of progesterone(Prog) target cells. The spayed 13 rats(Wistar, approximately 300gm) were randomly alloted into 3 groups. One group was the control group and another Prog-treated group was injected with 1mg of Prog/rat/day for 2 consecutive days, and Estand Prog-treated group was injected intramuscularly with $17{\beta}$-estradiol $20{\mu}g/rat/day$ for 3 consecutive days and then with Prog for 2 days as above from 4th day. Rats were administrated intraperitoneally with bromodeoxyuridinc(Brdur,0.2mg/BW once) befero 2 hours of exanguination. In gross finding, the groups with more level of dimension and weight on the uterus were ordered as Est- and Prog-treated group, Prog-treated group and control group. The investigation by immunohistochemical methods using paraffin sections of the uteri was performed by using anti-Brdur antibody for labeling proliferating cells of Prog target cells. The groups with higher labeling index(LI) were ordered as Prog-treated grop, Est- and Prog- treated group and control group. The number of proliferating cells from Prog target cells in the rats were rather deceased by Prog injection following Est injection than prog injection only. The cell types with higher LI in the wall layers of all 3 groups were ordered as endometrial stromal cells, glandular epithelial cells, luminal epithelial cells, myometrial muscle cells and serosa methodelial cells, and the region with highest LI was functional zone of the endometrium and the region with lower LI was muscular layer and then those with lowest LI was serosa and also the considerable different LI from individual rat were observed.
Objectives: Direct pulp capping is a treatment for mechanically exposed pulp in which a biocompatible capping material is used to preserve pulpal vitality. Biocompatibility tests in animal studies have used a variety of experimental protocols, particularly with regard to the exposure site. In this study, pulp exposure on the occlusal and mesial surfaces of molar teeth was investigated in a rat model. Materials and Methods: A total of 58 maxillary first molars of Wistar rats were used. Forty molars were mechanically exposed and randomly assigned according to 3 factors: 1) the exposure site (occlusal or mesial), 2) the pulp-capping material (ProRoot White MTA or Bio-MA), and 3) 2 follow-up periods (1 day or 7 days) (n = 5 each). The pulp of 6 intact molars served as negative controls. The pulp of 12 molars was exposed without a capping material (n = 3 per exposure site for each period) and served as positive controls. Inflammatory cell infiltration and reparative dentin formation were histologically evaluated at 1 and 7 days using grading scores. Results: At 1 day, localized mild inflammation was detected in most teeth in all experimental groups. At 7 days, continuous/discontinuous calcified bridges were formed at exposure sites with no or few inflammatory cells. No significant differences in pulpal response according to the exposure site or calcium-silicate cement were observed. Conclusions: The location of the exposure site had no effect on rat pulpal healing. However, mesial exposures could be performed easily, with more consistent results. The pulpal responses were not significantly different between the 2 capping materials.
Arun Kumar Tiwari;Pushpraj S Gupta;Mahesh Prasad;Paraman Malairajan
Journal of Pharmacopuncture
/
v.25
no.4
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pp.369-381
/
2022
Objectives: Hyperlipidemia (HL) is a major cause of ischemic heart diseases. The size-limiting effect of ischemic preconditioning (IPC), a cardioprotective phenomenon, is reduced in HL, possibly because of the opening of the mitochondrial permeability transition pore (MPTP). The objective of this study is to see what effect pretreatment with Inula racemose Hook root extract (IrA) had on IPC-mediated cardioprotection on HL Wistar rat hearts. An isolated rat heart was mounted on the Langendorff heart array, and then ischemia reperfusion (I/R) and IPC cycles were performed. Atractyloside (Atr) is an MPTP opener. Methods: The animals were divided into ten groups, each consisting of six rats (n = 6), to investigate the modulation of I. racemosa Hook extract on cardioprotection by IPC in HL hearts: Sham control, I/R Control, IPC control, I/R + HL, I/R + IrA + HL, IPC + HL, IPC + NS + HL, IPC + IrA+ HL, IPC + Atr + oxidative stress, mitochondrial function, integrity, and hemodynamic parameters are evaluated for each group. Results: The present experimental data show that pretreatment with IrA reduced the LDH, CK-MB, size of myocardial infarction, content of cardiac collagen, and ventricular fibrillation in all groups of HL rat hearts. This pretreatment also reduced the oxidative stress and mitochondrial dysfunction. Inhibition of MPTP opening by Atr diminished the effect of IrA on IPC-mediated cardioprotection in HL rats. Conclusion: The study findings indicate that pretreatment with IrA e restores IPC-mediated cardioprotection in HL rats by inhibiting the MPTP opening.
Colon cancer is the third most common malignant neoplasm in the world and it remains an important cause of death, especially in western countries. The toxic environmental pollutant, 1, 2-dimethylhydrazine (DMH), is also a colon-specific carcinogen. Tannic acid (TA) is reported to be effective against various types of chemically induced toxicity and also carcinogenesis. In the present study, we evaluated the chemopreventive efficacy of TA against DMH induced colon toxicity in a rat model. Efficacy of TA against the colon toxicity was evaluated in terms of biochemical estimation of antioxidant enzyme activities, lipid peroxidation, histopathological changes and expression of early molecular markers of inflammation and tumor promotion. DMH treatment induced oxidative stress enzymes (p<0.001) and an early inflammatory and tumor promotion response in the colons of Wistar rats. TA treatment prevented deteriorative effects induced by DMH through a protective mechanism that involved reduction of oxidative stress as well as COX-2, i-NOS, PCNA protein expression levels and TNF-${\alpha}$ (p<0.001) release. It could be concluded from our results that TA markedly protects against chemically induced colon toxicity and acts plausibly by virtue of its antioxidant, anti-inflammatory and antiproliferative activities.
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