The first part of this study reviewed the characteristics of calcium hydroxide ($Ca(OH)_2$) and summarized the results of in vitro studies related to its antimicrobial effects. The second part of this review covers in vivo studies including human clinical studies and animal studies. The use of $Ca(OH)_2$ as an intracanal medicament represented better histological results in animal studies. However, human clinical studies showed limited antimicrobial effects that microorganisms were reduced but not eliminated through the treatment, and that some species had resistance to $Ca(OH)_2$. Most of clinical outcome studies supported that there is no improvement in healing of periapical lesions when $Ca(OH)_2$ was applied between appointments. Further studies are required for the antimicrobial effects of $Ca(OH)_2$, and search for the ideal material and technique to completely clean infected root canals should be continued.
Kim, Dae-Geun;Kim, Hyo-Won;Kim, Jung-Hyun;Lee, Bae-Ik;Hong, Sun-Mee;Min, Kwan-Sik;Myung, Jeong-In;Kim, Dae-Jung
Korean Journal of Fisheries and Aquatic Sciences
/
v.50
no.6
/
pp.770-776
/
2017
This study investigated the effects of recombinant eel gonadotropin hormone (rJeGTH) produced in silkworms, with and without a carboxyl-terminal peptide from equine chorionic gonadotropin (eCG), on the induction of sexual maturation in female eels Anguilla japonica. Experiments were conducted both in vivo and in vitro. In in vitro trials, germinal vesicle breakdown (GVBD) induction did not significantly differ between rJeFSH and $rJeFSH{\cdot}eCG$ treatments and the control group. However, previous studies did find that rJeLH and $rJeLH{\cdot}eCG$ treatments induced GVBD in female eels. Our in vitro exploration of $estradiol-17{\beta}$ ($E_2$) levels in immature ovarian tissues revealed significantly higher $E_2$ levels in the group treated with $rJeFSH{\cdot}eCG$$1{\mu}g/mL$ than in the control group. In contrast, the in vivo experiments showed no effect of recombinant hormones on the sexual maturation of feminized eels. Previous studies and our own in vitro results have clearly shown that rJeGTH and $rJeGTH{\cdot}eCG$ have a positive effect on the sexual maturation of feminized eels. To develop the activity of rJeGTH in vivo, further studies should confirm circulation time and activity of these hormones in eels' bloodstream, modify the structure of the recombinant gene, and implement additional glycosylation.
Lopez, Ruth Mery;Lopez, Jorge Skiold;Lozano, Jair;Flores, Hector;Carranza, Rosa Angelica;Franco, Antonio;Castillo, Enrique Fernando
The Korean Journal of Physiology and Pharmacology
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v.24
no.4
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pp.339-348
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2020
We aimed to characterize the participation of rapid non-genomic and delayed non-genomic/genomic or genomic mechanisms in vasoactive effects to triiodothyronine (T3), emphasizing functional analysis of the involvement of these mechanisms in the genesis of nitric oxide (NO) of endothelial or muscular origin. Influences of in vitro and in vivo T3 treatments on contractile and relaxant responsiveness of isolated rat aortas were studied. In vivo T3-treatment was 500 ㎍·kg-1·d-1, subcutaneous injection, for 1 (T31d) and 3 (T33d) days. In experiments with endothelium-intact aortic rings contracted with phenylephrine, increasing concentrations of T3 did not alter contractility. Likewise, in vitro T3 did not modify relaxant responses induced by acetylcholine or sodium nitroprusside (SNP) nor contractile responses elicited by phenylephrine or angiotensin II in endothelium-intact aortas. Concentration-response curves (CRCs) to acetylcholine and SNP in endothelium-intact aortic rings from T31d and T33d rats were unmodified. T33d, but not T31d, treatment diminished CRCs to phenylephrine in endothelium-intact aortic rings. CRCs to phenylephrine remained significantly depressed in both endothelium-denuded and endothelium-intact, nitric oxide synthase inhibitor-treated, aortas of T33d rats. In endothelium-denuded aortas of T33d rats, CRCs to angiotensin II, and high K+ contractures, were decreased. Thus, in vitro T3 neither modified phenylephrine-induced active tonus nor CRCs to relaxant and contractile agonists in endothelium-intact aortas, discarding rapid non-genomic actions of this hormone in smooth muscle and endothelial cells. Otherwise, T33d-treatment inhibited aortic smooth muscle capacity to contract, but not to relax, in an endothelium- and NO-independent manner. This effect may be mediated by delayed non-genomic/genomic or genomic mechanisms.
The Journal of the Korean Society for Microbiology
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v.7
no.1
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pp.29-41
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1972
To grow Myocbacterium leprae in cultured mouse peritoneal macrophages, studies were made with trypsin-purified Myco. laprae on 1) the dynamics of infection of mouse peritonal macrophages in vivo with Myco. leprae by intraperitoneal inoculation, 2) growth experiment of Myco. leprae in cultured mouse peritoneal macrophages by in vivo infection and in vitro cultivation and 3) the observation of pathological changes in spleens of mice induced by intraperitoneal inoculation of Myco. leprae. Results are summarized as follows; 1. Continuing and significant decreases were observed in the numbers of both acid-fast bacilli in cultured macrophage and of macrophages harboring.acid-fast bacilli by the length of inter vats between the time of intraperitoneal inoculation of Myco. leprae and the time of initiation of macrophage culture. 2. No evidence of multiplication of Myco. leprae in the peritoneal macrophages in vivo was found up to 5 months after intraperitoneal inoculation. 3. With cultures of macrophages made 24 hours and 1 week after intraperitoneal inoculation of Myco. leprae and maintained in vitro up to 2 to 3 months, microscopic examination of the stained preparations of cultured macrophages indicated that an apparent increase in the number of acid-fast bacilli in the macrophages did occur. 4. Quantitative experiment with in vivo infected-in vitro cultured macrophages revealed certain features of increase in the number of total acid-fast bacilli in the cultured macrophages 7 and 9 weeks after initiation of the cultures. 5. Pathological changes in the spleens mice inoculated with Myco. leprae were of mainly degenerative nature in the red pulp. No multiplication of Myco. leprae was observed in the spleens of mice up to 5 months after intraperitoneal inoculation.
In 1951, Colin Russell Austin and Min Chueh Chang identified "capacitation", a special process involving ejaculated spermatozoa in the female reproductive tract. Capacitation is a phenomenon that occurs in vivo, but almost all knowledge of capacitation has been obtained from in vitro studies. Therefore, numerous trials have been performed to establish in vitro capacitation methods for various studies on reproduction. Although a series of studies have been conducted to develop an optimal protocol for inducing capacitation, most have focused on identifying the appropriate chemical compounds to induce the capacitation of boar spermatozoa in vitro. Therefore, the purpose of this study was to identify the optimal incubation time for inducing capacitation in vitro. Duroc semen was incubated for various periods (60, 90, and 120 min) to induce capacitation. Sperm function (sperm motility, motion kinematic parameters, and capacitation status) was evaluated. The results showed that total sperm motility, rapid sperm motility, progressive sperm motility, curvilinear velocity, and average path velocity significantly decreased in a time-dependent manner. However, the capacitation status did not show any significant changes. Taken together, these results indicate that an incubation time of more than 60 min suppresses sperm motility and motion kinematic parameters. Therefore, we suggest that 60 min may be the best incubation time to induce capacitation without negative effects on sperm motility and motion kinematics in boar spermatozoa in vitro.
Ginseng has been reported to reduce the risk of cancer in diverse organs, including the lip, oral cavity, pharynx, larynx, esophagus, lung, liver, pancreas, ovary, colon, rectum, and stomach, as demonstrated in clinical and epidemiological studies. studies, base on which findings, Panax ginseng has been classified as a "non-organ-specific cancer preventive." However, the recent keen interest in traditional medicinal herbs has been frequently questioned, about exact mode of action and the use of panaceic compounds has been a prime issue discussed in terms of complementary and alternative medicine. Several in vitro and in vivo studies have shown the mitigating effects of Korean red ginseng on Helicobacter pylori (H. pylori)-associated atrophic changes and carcinogenesis; However, evidence-based medicine, consisting of large-scale or well designed clinical studies, is still warranted whether Korean red ginseng is to be recognized as an essential therapeutic strategy regarding a "H. pylori-associated gastric cancer preventive." Specifically, comprehensive clinical trials of Korean red ginseng are needed to demonstrate that mucosal regeneration in patients with atrophic gastritis is feasible using Korean red ginseng supplements after the eradication of H. pylori infection. Ginseng is a good example of a natural herb and its ubiquitous properties may include the reduction or delay of inflammation carcinogenesis. Korean red ginseng contains ample amounts of active ginsenosides and we have demonstrated their effects in in vitro and in vivo studies with positive outcomes. In this review, the quantitative and qualitative benefits of Korean red ginseng in the treatment of H. pylori infection are described.
Purpose: The consumption of noodles has increased domestically. However, noodles with high carbohydrate content can cause an increase in blood glucose compared with other foods. Therefore, in this study, Naengmyeon with high resistant starch was prepared for decreasing blood glucose by the addition of 0.5% citric acid (CN), 1% guar gum (GN) or 0.5% citric acid and 1% guar gum (CGN), and then it was incubated in a refrigerator for 3 days, and stored in a freezer for 1 month. Methods: The quality characteristics of these Naengmyeon noodles was evaluated based on total starch, resistant starch, water absorption, cooking loss, turbidity, in vitro starch hydrolysis, and in vivo glucose response. Results: There was no significant difference in the total starch, cooking loss, and turbidity. The resistant starch of GN (1.70%) and CGN (1.84%) was significantly increased when compared with that in Naengmyeon with no additives (N) and CN. In terms of water absorption, CN (86.01%) was the lowest in samples, followed by GN (92.17%), N (94.20%), and CGN (99.16%). CGN with high resistant starch was the lowest in in vitro starch hydrolysis in samples. However, it had no effect on the in vivo glucose response. In vitro starch hydrolysis exhibited a significant positive correlation (r=0.533; p<0.01) with in vivo glucose response. Conclusion: Therefore, future studies are needed to establish the standard for resistant starch contents in processed carbohydrate foods for delaying the increase in blood glucose. If this standard is established, it might help to develop processed foods for diabetic patients.
Acetaminophen (APAP) overdose is known to cause severe hepatotoxicity mainly through the depletion of glutathione. In this study, we compared the cytotoxic effects of APAP on both a normal murine hepatic cell line, BNL CL.2, and its SV40-transformed cell line, BNL SV A.8. Gene expression profiles for APAP-treated cells were also obtained using microarray and analyzed to identify differences in genes or profiles that may explain the differences of susceptibility to APAP in these cell lines. These two cell lines exhibited different susceptibilities to APAP (0-$5,000{\mu}M$); BNL SV A.8 cells were more susceptible to APAP treatment compared to BNL CL.2 cells. A dose of $625{\mu}M$ APAP, which produced significant differences in cytotoxicity in these cell lines, was tested. Microarray analysis was performed to identify significant differentially expressed genes (DEGs) irrespective of APAP treatment. Genes up-regulated in BNL SV A.8 cells were associated with immune response, defense response, and apoptosis, while down-regulated genes were associated with catalytic activity, cell adhesion and the cytochrome P450 family. Consistent with the cytotoxicity data, no significant DEGs were found in BNL CL.2 cells after treatment with $625{\mu}M$ APAP, while cell cycle arrest and apoptosis-related genes were up-regulated in BNL SV A.8 cells. Based on the significant fold-changes in their expression, a genes were selected and their expressions were confirmed by quantitative real-time RT-PCR; there was a high correlation between them. These results suggest that gene expression profiles may provide a useful method for evaluating drug sensitivity of cell lines and eliciting the underlying molecular mechanism. We further compared the genes identified from our current in vitro studies to the genes previously identified in our lab as regulated by APAP in both C57BL/6 and ICR mice in vivo. We found that a few genes are regulated in a similar pattern both in vivo and in vitro. These genes might be useful to develop as in vitro biomarkers for predicting in vivo hepatotoxicity. Based on our results, we suggest that gene expression profiles may provide useful information for elucidating the underlying molecular mechanisms of drug susceptibility and for evaluating drug sensitivity in vitro for extrapolation to in vivo.
Ginsenosides are among the most well-known traditional herbal medicines frequently used for the treatment of various symptoms in South Korea. The neuroprotective effects of ginsenoside $Rg_3$ (G-$Rg_3$) on cholesterol-oxide-(CO)-induced neurotoxicity were investigated through the analyses of rat brains. The recently accumulated reports show that ginseng saponins (GTS), the major active ingredients of Panax ginseng, have protective effects against neurotoxin insults. In the present study, the neuroprotective effects of G-$Rg_3$ on CO-induced hippocampal excitotoxicity were examined in vivo. The in-vitro studies using rat cultured hippocampal neurons revealed that G-$Rg_3$ treatment significantly inhibited CO-induced hippocampal cell death. G-$Rg_3$ treatment not only significantly reduced CO-induced DNA damage but also attenuated CO-induced apoptosis. The in-vivo studies that were conducted revealed that the intracerebroventricular (i.c.v.) pre-administration of G-$Rg_3$ significantly reduced i.c.v. CO-induced hippocampal damage in rats. To examine the mechanisms underlying the in-vitro and in-vivo neuroprotective effects of G-$Rg_3$ against CO-induced hippocampal excitotoxicity, the effect of G-$Rg_3$ on the CO-induced elevations of the apoptotic cells in cultured hippocampal cells was examined, and it was found that G-$Rg_3$ treatment inhibited CO-induced apoptosis. The histopathological evaluation demonstrated that G-$Rg_3$ significantly diminished the apoptosis in the hippocampus and also spared the hippocampal CA1, CA3, and dentate gyrus neurons. G-$Rg_3$ also significantly improved the CO-caused behavioral impairment. G-$Rg_3$ itself had no effect, however, on the CO-induced inhibition of succinate dehydrogenase activity (data not shown). These results collectively indicate the G-$Rg_3$-induced neuroprotection against CO in rat hippocampus. With regard to the wide use of G-$Rg_3$, this agent is potentially beneficial in treating CO-induced brain injury.
Imperatorin, a major bioactive furanocoumarin with multifunctions, can be used for treating neurodegenerative diseases. In this study, we investigated the characteristics of imperatorin transport in the brain. Experiments of the present study were designed to study imperatorin transport across the blood-brain barrier both in vivo and in vitro. In vivo study was performed in rats using single intravenous injection and in situ carotid artery perfusion technique. Conditionally immortalized rat brain capillary endothelial cells were as an in vitro model of blood-brain barrier to examine the transport mechanism of imperatorin. Brain distribution volume of imperatorin was about 6 fold greater than that of sucrose, suggesting that the transport of imperatorin was through the blood-brain barrier in physiological state. Both in vivo and in vitro imperatorin transport studies demonstrated that imperatorin could be transported in a concentration-dependent manner with high affinity. Imperatorin uptake was dependent on proton gradient in an opposite direction. It was significantly reduced by pretreatment with sodium azide. However, its uptake was not inhibited by replacing extracellular sodium with potassium or N-methylglucamine. The uptake of imperatorin was inhibited by various cationic compounds, but not inhibited by TEA, choline and organic anion substances. Transfection of plasma membrane monoamine transporter, organic cation transporter 2 and organic cation/carnitine transporter 2/1 siRNA failed to alter imperatorin transport in brain capillary endothelial cells. Especially, tramadol, clonidine and pyrilamine inhibited the uptake of [$^3H$]imperatorin competitively. Therefore, imperatorin is actively transported from blood to brain across the blood-brain barrier by passive and carrier-mediated transporter.
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