tretinoin has been researched along with Reperfusion-Injury* in 14 studies
1 review(s) available for tretinoin and Reperfusion-Injury
1 trial(s) available for tretinoin and Reperfusion-Injury
13 other study(ies) available for tretinoin and Reperfusion-Injury
Article | Year |
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Possible Underlying Mechanisms for the Renoprotective Effect of Retinoic Acid-Pretreated Wharton's Jelly Mesenchymal Stem Cells against Renal Ischemia/Reperfusion Injury.
Objectives: The current work investigated the effect of Wharton jelly mesenchymal stem cells (WJ-MSCs) pretreated with all-trans-retinoic acid (ATRA) on renal ischemia in rats and the possible role of oxidative stress, apoptotic and Wnt/β-Catenin signaling pathways, and inflammatory cytokines in their effects. Methods: The study included 90 male Sprague Dawley rats that were allocated to five groups (n = 18 rats): (I) Sham-operated group (right nephrectomy was performed); (II) Ischemia/reperfusion injury (IRI) group, a sham group with 45-min renal ischemia on the left kidney; (III) ATRA group, an ischemic group with an intravenous (i.v.) administration of ATRA 10 µM, 10 min post-surgery); (IV) WJ-MSCs group, an IRI group with an i.v. administration of 150 µL containing 7 × 106 WJ-MSCs, 10 min post-surgery; (V) WJ-MSCs + ATRA group, an IRI group with an i.v. administration of 150 µL of 7 × 106 WJ-MSCs pretreated with 10 µM ATRA. At the end of the experiments, serum creatinine, BUN micro-albuminuria (MAU), urinary protein, markers of redox state in the left kidney (MDA, CAT, SOD, and GSH), and the expression of Bax, IL-6, HIF-1α, Wnt7B, and β-catenin genes at the level of mRNA as well as for immunohistochemistry for NFkB and β-Catenin markers were analyzed. Results: The current study found that 45-min of renal ischemia resulted in significant impairment of kidney function (evidenced by the increase in serum creatinine, BUN, and urinary proteins) and deterioration of the kidney morphology, which was associated with a significant increase in redox state (evidenced by an increase in MDA and a decrease in GSH, SOD, and CAT), and a significant increase in inflammatory and apoptotic processes (evidenced by an increase in Bax and IL-6, NFkB, Wnt7B, β-catenin and HIF-1α) in kidney tissues (p < 0.05). On the other hand, treatment with ATRA, WJ-MSCs, or a combination of both, caused significant improvement in kidney function and morphology, which was associated with significant attenuation of oxidative stress, apoptotic markers, and inflammatory cytokines (IL6 and NFkB) with the upregulation of HIF-1α and β-catenin in kidney tissues (p < 0.05). Moreover, the renoprotective effect of WJ-MSCs pretreated with ATRA was more potent than WJ-MSCs alone. Conclusions: It is concluded that preconditioning of WJ-MSCs with ATRA may enhance their renoprotective effect. This effect could be due to the upregulation of the beta-catenin/Wnt pathway and attenuation of apoptosis, infla Topics: Animals; bcl-2-Associated X Protein; beta Catenin; Creatinine; Cytokines; Interleukin-6; Ischemia; Kidney; Male; Mesenchymal Stem Cell Transplantation; Mesenchymal Stem Cells; NF-kappa B; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Superoxide Dismutase; Tretinoin; Wharton Jelly | 2022 |
Effects of ATRA on diabetic rats with renal ischemia-reperfusion injury.
To explore the role of all-trans retinoic acid (ATRA) in renal ischemia/reperfusion injury of diabetic rats.. Sixty adult male rats were randomly divided into 6 groups, including sham group (S group), ischemia-reperfusion group (I/R group), ischemia-reperfusion+ATRA group (A group), diabetic group (D group), diabetic ischemia-reperfusion group (DI/R group), diabetic ischemia-reperfusion +ATRA group (DA group). The levels of creatinine (Cr), cystatin C (Cys-C) and β2-microglobulin (β2-MG) were measured. Morphology of renal tissue was observed under light microscope.. DJ-1, Nrf2, HO-1 and caspase-3 were detected by western blot. DJ-1, Nrf2, HO-1 and caspase-3 in I/R group, D group and DI/R group was higher than that in S group. Compared with I/R group, Nrf2 and HO-1 in A group was decreased, but caspase-3 was increased. However, Nrf2 in DA group was higher than that in DI/R group, HO-1 and caspase-3 in DA group were lower than that in DI/R group. Compared with group S, Cr, Cys-C and β2-MG in I/R group, A group, D group, and DI/R group were higher. Whereas the levels of Cr, Cys-C, β2-MG and renal injury score in DA group were lower than those in DI/R group.. ATRA has a protective effect on renal ischemia-reperfusion injury in diabetic rats, maybe relating to DJ/Nrf2 pathway. Topics: Animals; Diabetes Mellitus, Experimental; Disease Models, Animal; Drug Evaluation, Preclinical; Kidney; Male; NF-E2-Related Factor 2; Rats; Reperfusion Injury; Streptozocin; Tretinoin | 2020 |
ATRA Regulates Innate Immunity in Liver Ischemia/Reperfusion Injury via RARα/Akt/Foxo1 Signaling.
All-trans retinoic acid (ATRA) has been proved to protect liver from ischemia/reperfusion (IR) injury, however, its mechanism is still unclear. This study is to investigate the mechanism of effect of ATRA on innate immunity in mice liver IR injury. Before operation, mice were gavaged by ATRA at 15 mg/kg/d for two weeks, and then the liver was underwent 70% ischemia (90 min) and reperfusion (6 h). Liver function was assessed by serum alanine aminotransferase (sALT), serum aspartate aminotransferase (sAST). Real-time PCR and Western blot were to detect the level of mRNA and protein. In vitro, RAW264.7 macrophages were treatment with ATRA (1 µM) or LE540 (5 µM, a retinoic acid receptor α (RARα) receptor antagonist) before lipopolysaccharide (100 ng/mL) stimulation. In vivo, ATRA protected the liver from IR injury by improving hepatocellular function (sALT and sAST), decreasing cell apoptosis and inhibiting inflammatory response (i.e., the level of toll-like receptor 4, transcription factor nuclear factor-κBp65, interleukin (IL)-1β, IL-6, and tumor necrosis factor-α). When RARα was blocked by LE540 in RAW264.7 macrophages, the inflammatory cytokines were enhancing, along with a decline of Akt phosphorylation but Forkhead box o (Foxo) 1, compared with the ATRA group. In summary, ATRA regulates in part the innate immunity to protect liver from IR injury by RARα/Akt/Foxo1 pathway. Topics: Animals; Apoptosis; Cytokines; Forkhead Box Protein O1; Immunity, Innate; Liver; Male; Mice; Mice, Inbred C57BL; Protective Agents; Proto-Oncogene Proteins c-akt; RAW 264.7 Cells; Reperfusion Injury; Retinoic Acid Receptor alpha; RNA, Messenger; Signal Transduction; Toll-Like Receptor 4; Transcription Factor RelA; Tretinoin | 2018 |
All-Trans Retinoic Acid Ameliorates the Early Experimental Cerebral Ischemia-Reperfusion Injury in Rats by Inhibiting the Loss of the Blood-Brain Barrier via the JNK/P38MAPK Signaling Pathway.
All-trans retinoic acid (ATRA) influences the outcomes of cerebral ischemic reperfusion (CIR) injury, but the mechanism remains unclear. The present study aimed to investigate the effects of ATRA on loss of the blood brain barrier (BBB) following CIR and to explore the possible mechanisms. Transient middle cerebral artery occlusion was performed on male SD rats to construct an in vivo CIR model. Neurological deficits, BBB permeability, brain edema, MRI and JNK/P38 MAPK proteins were detected at 24 h following CIR. We demonstrated that ATRA pretreatment could alleviate CIR-induced neurological deficits, increase of BBB permeability, infarct volume, degradation of tight junction proteins, inhibit MMP-9 protein expression and activity. ATRA treatment also reduced the p-P38 and p-JNK protein level. However the protective effect of ATRA on CIR could be reversed by administration of retinoic acid alpha receptor antagonist Ro41-5253. SP600125 and SB203580, which is the JNK/P38 pathway inhibitors has the same protective effect as ATRA. These results indicated that ATRA may inhibit the JNK/P38 MAPK pathway to alleviate BBB disruption and improve CIR outcomes. Topics: Animals; Blood-Brain Barrier; Brain Ischemia; Dose-Response Relationship, Drug; Male; MAP Kinase Signaling System; p38 Mitogen-Activated Protein Kinases; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Time Factors; Tretinoin | 2018 |
Ginsenoside Rb1 Treatment Attenuates Pulmonary Inflammatory Cytokine Release and Tissue Injury following Intestinal Ischemia Reperfusion Injury in Mice.
Objective. Intestinal ischemia reperfusion (II/R) injury plays a critical role in remote organ dysfunction, such as lung injury, which is associated with nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway. In the present study, we tested whether ginsenoside Rb1 attenuated II/R induced lung injury by Nrf2/HO-1 pathway. Methods. II/R injury was induced in male C57BL/6J mice by 45 min of superior mesenteric artery (SMA) occlusion followed by 2 hours of reperfusion. Ginsenoside Rb1 was administrated prior to reperfusion with or without ATRA (all-transretinoic acid, the inhibitor of Nrf2/ARE signaling pathway) administration before II/R. Results. II/R induced lung histological injury, which is accompanied with increased levels of malondialdehyde (MDA), interleukin- (IL-) 6, and tumor necrosis factor- (TNF-) α but decreased levels of superoxide dismutase (SOD) and IL-10 in the lung tissues. Ginsenoside Rb1 reduced lung histological injury and the levels of TNF-α and MDA, as well as wet/dry weight ratio. Interestingly, the increased Nrf2 and HO-1 expression induced by II/R in the lung tissues was promoted by ginsenoside Rb1 treatment. All these changes could be inhibited or prevented by ATRA. Conclusion. Ginsenoside Rb1 is capable of ameliorating II/R induced lung injuries by activating Nrf2/HO-1 pathway. Topics: Animals; Ginsenosides; Heme Oxygenase-1; Interleukin-10; Interleukin-6; Intestines; Lung; Male; Malondialdehyde; Mice; Mice, Inbred C57BL; NF-E2-Related Factor 2; Reperfusion Injury; Signal Transduction; Superoxide Dismutase; Tretinoin; Tumor Necrosis Factor-alpha | 2015 |
Retinoic acid receptor α promotes autophagy to alleviate liver ischemia and reperfusion injury.
To study the role of autophagy and the relationship between retinoic acid receptor α (RARα) and autophagy in liver ischemia and reperfusion (IR) injury.. All-trans retinoic acid (ATRA) was administered to mice for two weeks before operation. Reverse transcription-polymerase chain reaction and Western blot were used to detect the expression levels of related factors. To demonstrate the role of RARα, LE540, a RARα inhibitor, was used to treat hepatocytes injured by H2O2 in vitro.. ATRA pretreatment noticeably diminished levels of serum alanine aminotransferase and aspartate aminotransferase as well as the degree of histopathological changes. Apoptosis was also inhibited, whereas autophagy was promoted. In vitro, RARα was inhibited by LE540, which resulted in decreased autophagy and increased apoptosis. Similarly, the expression of Foxo3a and p-Akt was downregulated, but Foxo1 expression was upregulated.. This research provides evidence that ATRA can protect the liver from IR injury by promoting autophagy, which is dependent on Foxo3/p-Akt/Foxo1 signaling. Topics: Animals; Apoptosis; Autophagy; Cytoprotection; Dibenzazepines; Disease Models, Animal; Forkhead Box Protein O1; Forkhead Box Protein O3; Forkhead Transcription Factors; Hepatocytes; Hydrogen Peroxide; Liver; Liver Diseases; Male; Mice, Inbred C57BL; Oxidative Stress; Phosphorylation; Proto-Oncogene Proteins c-akt; Receptors, Retinoic Acid; Reperfusion Injury; Retinoic Acid Receptor alpha; Signal Transduction; Time Factors; Tretinoin | 2015 |
Protective effect of ginsenoside Rb1 against intestinal ischemia-reperfusion induced acute renal injury in mice.
Ginsenoside Rb1 (RB1), the most clinically effective constituent of ginseng, possesses a variety of biological activities. The objectives of this study were to investigate the protective effects of RB1 and its underlying mechanism on renal injury induced by intestinal ischemia-reperfusion (IIR) in mice. RB1 was administered prior to inducing IIR achieved by occluding the superior mesenteric artery for 45 min followed by 120 min of reperfusion. All-trans-retinoic acid (ATRA) was used as an inhibitor of NF-E2-related factor-2 (Nrf2) signaling. Adult male C57BL/6J mice were randomly divided into six groups: (1) sham group, (2) IIR group, (3) RB1 group, (4) sham + ATRA group, (5) IIR + ATRA group, and (6) RB1 + ATRA group. Intestinal histology and pathological injury score were observed. Intestinal mucosal injury was also evaluated by measuring serum diamine oxidase (DAO). Renal injury induced by IIR was characterized by increased levels of histological severity score, blood urea nitrogen (BUN), serum creatinine (Scr) and neutrophil gelatinase-associated lipocalin (NGAL), which was accompanied with elevated renal TUNEL-positive cells and the Bcl-2/Bax expression ratio. RB1 significantly reduced renal injury and apoptosis as compared with IIR group, which was reversed by ATRA treatment. Immunohistochemistry and Western blot analysis demonstrated that RB1 significantly upregulated the protein expression of heme oxygenase-1 (HO-1) and Nrf2, which were attenuated by ATRA treatment. Taken together, these results suggest that the protective effects of RB1 pretreatment against renal injury induced by IIR are associated with activation of the Nrf2/ anti-oxidant response element (ARE) pathway. Topics: Acute Kidney Injury; Acute-Phase Proteins; Amine Oxidase (Copper-Containing); Animals; Antioxidants; bcl-2 Homologous Antagonist-Killer Protein; bcl-2-Associated X Protein; Blood Urea Nitrogen; Creatinine; Gene Expression Regulation; Ginsenosides; Intestinal Mucosa; Intestines; Kidney; Lipocalin-2; Lipocalins; Male; Mice; Mice, Inbred C57BL; NF-E2-Related Factor 2; Oncogene Proteins; Oxidative Stress; Reperfusion Injury; Signal Transduction; Tretinoin | 2013 |
All-trans retinoic acid preconditioning protects against liver ischemia/reperfusion injury by inhibiting the nuclear factor kappa B signaling pathway.
Inflammatory response plays a pathogenic role in liver ischemia/reperfusion (I/R) injury. All-trans retinoic acid (ATRA) is an active metabolite of vitamin A with anti-inflammatory effects. However, there are few reports on the anti-inflammatory effects of ATRA on liver I/R injury. The purpose of this study was to investigate the effects of ATRA on liver I/R injury and related mechanisms.. A total of 54 male Sprague-Dawley rats were randomly divided into three groups (18 rats each), namely, sham, I/R, and I/R+ATRA groups. ATRA was intraperitoneally administered at a dose of 15mg/kg/d 14d before ischemia surgery. The segmental (70%) hepatic ischemia model was used by clamping the portal vein, hepatic artery, and bile duct of the left and median for 1h. The rats were sacrificed 3, 6, and 24h after reperfusion, and blood and liver tissue samples were obtained. Liver injury was evaluated by biochemical and histopathologic examinations. Myeloperoxidase activity was spectrophotometrically measured. The expression of pro-inflammatory cytokines, such as tumor necrosis factor-α and interleukin-6 was measured by enzyme-linked immunosorbent assay and real-time polymerase chain reaction. Liver nuclear factor kappa B (NF-κB) was detected by immunohistochemistry. The expression of NF-κB p65 and inhibitor NF-κB-α (IκBα) was determined by Western blot analysis.. The serum alanine aminotransferase level, Suzuki scores of hepatic histology, and hepatic myeloperoxidase activity, as indices of hepatic injury, were increased after reperfusion. The increase was attenuated by preadministration with ATRA. Compared with the I/R group, ATRA treatment increased IκBα expression and suppressed NF-κB p65 expression. Subsequently, the levels of tumor necrosis factor-α and interleukin-6 after liver I/R were effectively downregulated.. ATRA administration can significantly attenuate I/R injury in rat liver. The protective mechanism is related to its anti-inflammatory function of inhibiting NF-κB activation. Topics: Animals; Interleukin-6; Ischemic Preconditioning; Liver; Male; NF-kappa B; Peroxidase; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Signal Transduction; Tretinoin; Tumor Necrosis Factor-alpha | 2013 |
Electroacupuncture promotes neurological functional recovery via the retinoic acid signaling pathway in rats following cerebral ischemia-reperfusion injury.
Neurogenesis is regulated by a number of signaling pathways, including the retinoic acid (RA) pathway, a key regulator of neurogenesis in the subventricular zone (SVZ) and hippocampus. Acupuncture has been used to treat neurological conditions and is known to potentially enhance cell proliferation in the neurogenic area (hippocampal dentate gyrus and the SVZ of the lateral ventricle walls) in pathological conditions, which is associated with improved brain function. However, whether or not the neuroprotective effects of electroacupuncture (EA) are mediated by the regulation of the RA signaling pathway remains to be determined. Using a transient middle cerebral artery occlusion model, in the present study we evaluated the effect of EA on the neurological functional recovery, infarction volume and investigated the underlying molecular mechanisms. Two hundred and sixteen SD rats were randomly divided into 3 groups: sham, model group (ischemic rats without EA stimulation) and EA group (ischemic rats with EA stimulation on ST36 and LI11). Behavioral deficits were detected with high-resolution digital analysis of 24-h home-cage video recordings. Infarct volume was determined by triphenyltetrazolium hydrochloride staining and the expression of RA mRNA and protein was measured using RT-PCR and western blotting, respectively. We found that EA decreased the infarct volume, promoted neurological functional recovery and increased the RA mRNA and protein expression, compared with the model group. Findings of this study suggest that promoting neurological functional recovery by modulating RA expression in the post-ischemic brain is one of the mechanisms by which EA can be effective in the treatment of ischemic stroke. Topics: Animals; Brain; Brain Ischemia; Cell Proliferation; Disease Models, Animal; Electroacupuncture; Hippocampus; Infarction, Middle Cerebral Artery; Lateral Ventricles; Male; Neurogenesis; Rats; Rats, Sprague-Dawley; Recovery of Function; Reperfusion Injury; Signal Transduction; Stroke; Tetrazolium Salts; Tretinoin | 2013 |
Orphan nuclear receptor Nur77 promotes acute kidney injury and renal epithelial apoptosis.
Nur77 and its family members Nurr1 and Nor-1 are inducible orphan nuclear receptors that orchestrate cellular responses to diverse extracellular signals. In epithelia, Nur77 can act as a potent proapoptotic molecule in response to cellular stress, suggesting a possible role for this nuclear receptor in the tissue response to injury. Here, we found that Nur77 promotes epithelial cell apoptosis after AKI. Injury of proximal tubular epithelial cells rapidly and strongly induced Nur77, Nor-1, and Nurr1 both in vitro and in vivo. After renal ischemia-reperfusion, Nurr77-deficient mice exhibited less apoptosis of tubular epithelial cells and better renal function than wild-type mice. Nur77-mediated renal injury involved a conformational change of Bcl2 and an increase in the protein levels of proapoptotic Bcl-xS. Ligand-activated retinoic acid receptors repressed Nur77 induction and function. Pretreatment of wild-type mice with retinoic acid before renal ischemia-reperfusion blunted the induction of Nur77, conferred protection of renal function, attenuated renal histologic injury, and reduced the expression of epithelial-derived proinflammatory cytokines. Retinoic acid also inhibited hypoxia-mediated induction of proinflammatory cytokines in cultured renal epithelial cells. Results obtained from proximal tubule cultures derived from Nur77-deficient mice suggested that the inhibition of Nur77 expression mediated the renoprotective effects of retinoic acid. In summary, Nur77 promotes epithelial apoptosis after ischemia-reperfusion injury, and retinoic acid-mediated inhibition of Nur77 expression is a promising therapeutic strategy for the prevention of AKI. Topics: Acute Kidney Injury; Animals; Apoptosis; Cells, Cultured; Dimethyl Sulfoxide; Disease Models, Animal; DNA-Binding Proteins; Epithelial Cells; In Situ Hybridization; Kidney Function Tests; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Nuclear Receptor Subfamily 4, Group A, Member 1; Random Allocation; Reference Values; Reperfusion Injury; Severity of Illness Index; Tretinoin | 2012 |
All-trans retinoic acid alleviates hepatic ischemia/reperfusion injury by enhancing manganese superoxide dismutase in rats.
All-trans retinoic acid (atRA) is an active metabolite of vitamin A with antioxidant effects. There have been few reports on the effects of atRA on liver ischemia/reperfusion (I/R) injury. Here we have used a rat liver ischemia/ reperfusion model to analyze the protective effect of atRA. Rats were administered with different does (5-15 mg/kg/d) of atRA intraperitoneally (i.p.) for 14 d before I/R. Partial (70%) hepatic ischemia was induced by clamping the hepatic artery, portal vein, and bile duct to the left and median lobes of the liver using a vascular clamp for 60 min, followed by 24 h of reperfusion. The serum aminotransferase (ALT and AST) and hepatic pathology were used to evaluate I/R injury. The results demonstrate that atRA pretreatment attenuates liver I/R injury by inhibiting the release of malondialdehyde (MDA) and by enhancing the activity of superoxide dismutase (SOD). To gain insight into the mechanism of the SOD up-regulation by atRA, the activity of p38 mitogenactivated protein kinase (p38MAKP) and Akt was measured. The results showed that the phosphorylation of p38MAPK and Akt paralleled the expression of manganese superoxide dismutase (MnSOD). That these activities are related was demonstrated by the addition of a p38 inhibitor which markedly decreased MnSOD levels. Taken together, our data reveal that atRA can protect liver from I/R injury by increaseing MnSOD, which is associated with an increased activity of p38MAPK and Akt. Topics: Animals; Antioxidants; Disease Models, Animal; Liver; Liver Diseases; Male; Malondialdehyde; p38 Mitogen-Activated Protein Kinases; Phosphorylation; Proto-Oncogene Proteins c-akt; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Superoxide Dismutase; Tretinoin; Up-Regulation | 2010 |
Retinoic acids acting through retinoid receptors protect hippocampal neurons from oxygen-glucose deprivation-mediated cell death by inhibition of c-jun-N-terminal kinase and p38 mitogen-activated protein kinase.
Retinoic acids (RAs), including all-trans retinoic acid (ATRA) and 9-cis retinoic acid (9-cis RA), play fundamental roles in a variety of physiological events in vertebrates, through their specific nuclear receptors: retinoic acid receptor (RAR) and retinoid X receptor (RXR). Despite the physiological importance of RA, their functional significance under pathological conditions is not well understood. We examined the effect of ATRA on oxygen/glucose-deprivation/reperfusion (OGD/Rep)-induced neuronal damage in cultured rat hippocampal slices, and found that ATRA significantly reduced neuronal death. The cytoprotective effect of ATRA was observed not only in cornu ammonis (CA) 1 but also in CA2 and dentate gyrus (DG), and was attenuated by selective antagonists for RAR or RXR. By contrast, in the CA3 region, no protective effects of ATRA were observed. The OGD/Rep also increased phosphorylated forms of c-jun-N-terminal kinase (P-JNK) and p38 (P-p38) in hippocampus, and specific inhibitors for these kinases protected neurons. ATRA prevented the increases in P-JNK and P-p38 after OGD/Rep, as well as the decrease in NeuN and its shrinkage, all of which were inhibited by antagonists for RAR or RXR. These findings suggest that the ATRA signaling via retinoid receptors results in the inhibition of JNK and p38 activation, leading to the protection of neurons against OGD/Rep-induced damage in the rat hippocampus. Topics: Analysis of Variance; Animals; Blood Glucose; Cell Death; Enzyme Inhibitors; Hippocampus; Hypoxia; In Vitro Techniques; JNK Mitogen-Activated Protein Kinases; Neurons; p38 Mitogen-Activated Protein Kinases; Rats; Rats, Wistar; Receptors, Retinoic Acid; Reperfusion Injury; Signal Transduction; Statistics, Nonparametric; Tretinoin | 2007 |
[Experimental studies of effects of retinoic acid on the proliferation of retinal cells].
To determine whether the application of exogenous retinoic acid (RA) may induce the proliferation of retinal cells in adult rat.. Thirty-two healthy adult Sprague-Dawley (SD) rats were randomly divided into 4 groups. In Group 1 and Group 2, all-trans RA (5 microliter, 0.001 mol/L) was injected into the subretinal space. In Group 3 and Group 4, all-trans RA (10 microliter, 0.001 mol/L) was injected into epiretinal vitreous space. In the Group 1 and Group 3, transient ischemic-reperfusion injuries of the experimental eyes were induced by ligating ophthalmic artery prior to RA treatment. In the control group, 5 SD rats were treated by ischemia-reperfusion injuries but no exogenous RA application. The treated eyes were enucleated for light microscopic analysis and immunohistochemical assays after 2 - 4 weeks of RA application.. In group 1, the number of the retinal cells expressing rod-specific opsin marker in the subretinal space was significantly increased and the thickness of inner nuclear layer was also increased after the RA treatment for 16 days. However, no cell proliferation was detected in group 2. There were also no changes within population of retinal cells in Group 3 and Group 4 in which RA was injected into epiretinal vitreous space no matter under the ischemia-reperfusion or non-ischemia-reperfusion. In the control group, there were no significant morphological changes within the neural retinal layers as well as photoreceptor proliferation.. The application of RA in the subretinal space can induce photoreceptor proliferation in adult rat under an ischemic-reperfusion injury condition. It will provide a new idea for the regeneration of neural retinal cells. Topics: Animals; Biomarkers; Cell Division; Disease Models, Animal; Keratolytic Agents; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Retinal Rod Photoreceptor Cells; Rod Opsins; Tretinoin | 2002 |