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Sodium Ferulate Inhibits Neointimal Hyperplasia in Rat Balloon Injury Model  [PDF]
Jing Zhang, Jing Chen, Jian Yang, Changwu Xu, Jiawang Ding, Jun Yang, Qing Guo, Qi Hu, Hong Jiang
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0087561
Abstract: Background/Aim Neointimal formation after vessel injury is a complex process involving multiple cellular and molecular processes. Inhibition of intimal hyperplasia plays an important role in preventing proliferative vascular diseases, such as restenosis. In this study, we intended to identify whether sodium ferulate could inhibit neointimal formation and further explore potential mechanisms involved. Methods Cultured vascular smooth muscle cells (VSMCs) isolated from rat thoracic aorta were pre-treated with 200 μmol/L sodium ferulate for 1 hour and then stimulated with 1 μmol/L angiotensin II (Ang II) for 1 hour or 10% serum for 48 hours. Male Sprague-Dawley rats subjected to balloon catheter insertion were administrated with 200 mg/kg sodium ferulate (or saline) for 7 days before sacrificed. Results In presence of sodium ferulate, VSMCs exhibited decreased proliferation and migration, suppressed intracellular reactive oxidative species production and NADPH oxidase activity, increased SOD activation and down-regulated p38 phosphorylation compared to Ang II-stimulated alone. Meanwhile, VSMCs treated with sodium ferulate showed significantly increased protein expression of smooth muscle α-actin and smooth muscle myosin heavy chain protein. The components of Notch pathway, including nuclear Notch-1 protein, Jagged-1, Hey-1 and Hey-2 mRNA, as well as total β-catenin protein and Cyclin D1 mRNA of Wnt signaling, were all significantly decreased by sodium ferulate in cells under serum stimulation. The levels of serum 8-iso-PGF2α and arterial collagen formation in vessel wall were decreased, while the expression of contractile markers was increased in sodium ferulate treated rats. A decline of neointimal area, as well as lower ratio of intimal to medial area was observed in sodium ferulate group. Conclusion Sodium ferulate attenuated neointimal hyperplasia through suppressing oxidative stress and phenotypic switching of VSMCs.
Sodium-Glucose Cotransporter Inhibition Prevents Oxidative Stress in the Kidney of Diabetic Rats  [PDF]
Horacio Osorio,Israel Coronel,Abraham Arellano,Ursino Pacheco,Rocío Bautista,Martha Franco,Bruno Escalante
Oxidative Medicine and Cellular Longevity , 2012, DOI: 10.1155/2012/542042
Abstract: The hyperglycemia triggers several chronic diabetic complications mediated by increased oxidative stress that eventually causes diabetic nephropathy. The aim of this study was to examine if the sodium-glucose cotransporter (SGLT2) inhibition prevents the oxidative stress in the kidney of diabetic rats. Methods. The diabetic rat model was established by intraperitoneal injection of streptozotocin (50 mg/kg). The inhibition of SGLT2 was induced by daily subcutaneous administration of phlorizin (0.4 g/kg). Oxidative stress was assessed by catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD) activities and by immunohistochemical analysis of 3-nitrotyrosine (3-NT). Results. Streptozotocin-induced diabetes caused hyperglycemia and lower body weight. The CAT activity decreased in cortex and medulla from diabetic rats; in contrast, the GPx activity increased. Furthermore the 3-NT staining of kidney from diabetic rats increased compared to control rats. The inhibition of SGLT2 decreased hyperglycemia. However, significant diuresis and glucosuria remain in diabetic rats. The phlorizin treatment restores the CAT and GPX activities and decreases 3-NT staining. Conclusion. The inhibition of SGLT2 by phlorizin prevents the hyperglycemia and oxidative stress in kidney of diabetic rats, suggesting a prooxidative mechanism related to SGLT2 activity.
Sodium-Glucose Cotransporter Inhibition Prevents Oxidative Stress in the Kidney of Diabetic Rats  [PDF]
Horacio Osorio,Israel Coronel,Abraham Arellano,Ursino Pacheco,Rocío Bautista,Martha Franco,Bruno Escalante
Oxidative Medicine and Cellular Longevity , 2012, DOI: 10.1155/2012/542042
Abstract: The hyperglycemia triggers several chronic diabetic complications mediated by increased oxidative stress that eventually causes diabetic nephropathy. The aim of this study was to examine if the sodium-glucose cotransporter (SGLT2) inhibition prevents the oxidative stress in the kidney of diabetic rats. Methods. The diabetic rat model was established by intraperitoneal injection of streptozotocin (50?mg/kg). The inhibition of SGLT2 was induced by daily subcutaneous administration of phlorizin (0.4?g/kg). Oxidative stress was assessed by catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD) activities and by immunohistochemical analysis of 3-nitrotyrosine (3-NT). Results. Streptozotocin-induced diabetes caused hyperglycemia and lower body weight. The CAT activity decreased in cortex and medulla from diabetic rats; in contrast, the GPx activity increased. Furthermore the 3-NT staining of kidney from diabetic rats increased compared to control rats. The inhibition of SGLT2 decreased hyperglycemia. However, significant diuresis and glucosuria remain in diabetic rats. The phlorizin treatment restores the CAT and GPX activities and decreases 3-NT staining. Conclusion. The inhibition of SGLT2 by phlorizin prevents the hyperglycemia and oxidative stress in kidney of diabetic rats, suggesting a prooxidative mechanism related to SGLT2 activity. 1. Introduction Diabetic nephropathy (DN) is a leading cause of end-stage renal failure, accounting for 35% to 40% of all new cases that require dialysis therapy worldwide. Clinical studies have demonstrated that hyperglycemia is an important causal factor that mediates the development and progression of diabetic kidney disease [1]. Several evidences suggest that the controlling of glucose in the renal proximal tubular could play a major role in the genesis of diabetic systemic complications [2, 3]. On the other hand it has been shown that increases in glucose uptake in the kidney during diabetes could lead to high intracellular glucose levels, inducing an enhanced production of reactive oxygen species (ROS), which probably can be amplified by the decreased capacity of the cellular antioxidant defense system in this condition [4, 5]. Recently, we have reported increased sodium glucose cotransporter (SGLT2) activity and expression in rats with diabetes and salt sensitivity [6, 7]. Also, we showed that the increase in oxidative stress and SGLT2 expression was prevented by ursodeoxycholic acid treatment in diabetic rats [8]. The excessive production of ROS has been suggested as a common outcome from the
Reduction of voltage gated sodium channel protein in DRG by vector mediated miRNA reduces pain in rats with painful diabetic neuropathy
Munmun Chattopadhyay, Zhigang Zhou, Shuanglin Hao, Marina Mata, David J Fink
Molecular Pain , 2012, DOI: 10.1186/1744-8069-8-17
Abstract: Subcutaneous inoculation of the miRNA-expressing HSV vector into the feet of diabetic rats to transduce DRG resulted in a reduction in NaVα subunit levels in DRG neurons, coincident with a reduction in cold allodynia, thermal hyperalgesia and mechanical hyperalgesia.These data support the role of increased NaVα protein in DRG in the pathogenesis of pain in diabetic neuropathy, and provide a proof-of-principle demonstration for the development of a novel therapy that could be used to treat intractable pain in patients with diabetic neuropathy.Pain is a common complication of diabetic neuropathy that, despite substantial advances in understanding of pathophysiology, remains relatively refractory to treatment with available agents [1]. In rats with streptozotocin (STZ) induced diabetes and painful neuropathy, an increase in the alpha (pore-forming) subunit of voltage gated sodium channel isoform 1.7 (NaV1.7) in primary sensory afferent neurons of the dorsal root ganglia (DRG) has been reported [2], a change that correlates with increased amplitude and negative shift of the activation of tetrodotoxin (TTX)-sensitive current in those neurons. A potential pathogenic role for NaV1.7 in the development of pain in this syndrome is supported by the observation that gain of function mutations in NaV1.7 cause inherited spontaneous neuropathic pain syndromes primary erythermalgia [3,4] and paroxysmal extreme pain disorder [5].In previous studies we have constructed a series of herpes simplex virus (HSV)-based gene transfer vectors that effectively transduce DRG in vivo from skin inoculation, and have used these vectors to express inhibitory neurotransmitters [6-8] or neurotrophic factors [9-11]. In order to explicitly test the role of increased levels of NaV in DRG in the pathogenesis of pain in PDN, we constructed a non-replicating herpes simplex virus (HSV)-based vector to reduce NaVα protein in DRG, and compared the effect of NaVα subunit knockdown on pain-related behaviors i
Neurogenesis-enhancing effect of sodium ferulate and its role in repair following stress-induced neuronal damage  [PDF]
Lijian Yu, Yongping Zhang, Mingneng Liao, Yanping Wang, Rundi Ma, Xiaoyu Zhang, Tingxi Yu
World Journal of Neuroscience (WJNS) , 2011, DOI: 10.4236/wjns.2011.12002
Abstract: Ferulic acid (FA) is a ubiquitous phenolic acid of low toxicity, and sodium ferulate (SF) is its sodium salt. Our previous studies have revealed that FA shows neuroprotective effect and significant antidepressant- like effect. The aim of this study was to investigate its potential neurogenesis-enhancing effect and its role in repair following stress-induced neuronal damage. MTT assay was performed to measure the effect of SF on the growth of rat pheochromocytoma (PC12) cells; morphological and immunocytochemical meth- ods were used for assessing its differentiation-induc- ing action. Chronic mild stress (CMS) tests were per- formed to establish rat model of depression. The histopathology of animal brains was studied to ana- lyze CMS-induced morphological changes and the effect of SF on the repair of CMS-induced brain in- jury. The expressions of nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) and the proliferation of neural stem cell/neural progenitor cells were assessed in the hippocampi of chronic mild stress (CMS)-induced depression-like model rats by immunohistochemistry and bromodeoxyuridine (BrdU)- incorporation assays, respectively. Our in vitro tests showed that SF promoted the proliferation of PC12 cells in the concentration range of 5 - 320 μM, and induced PC12 cells to differentiate to more mature cells with the morphological characteristics and mo- lecular marker of neuronal-like cells. In vivo tests showed that SF up-regulated the expressions of NGF and BDNF, and induced the proliferation of neural stem cell/neural progenitor cells in the hippocampi of CMS-induced depression-like model rats. This study provides evidences that SF shows neurogenesis-en- hancing effect, and its antidepressant-like effect of SF may be related directly and closely to its above-men- tioned effect.
CARDIOPROTECTIVE EFFECT OF ESCULETIN ON CARDIAC MARKER ENZYMES AND MEMRANE BOUND ENZYMES IN ISOPROTERENOL-INDUCED MYOCARDIAL INFARCTION IN WISTAR RATS  [PDF]
Palanivel Karthika,Murugan Rajadurai,Palanisamy Ganapathy,Ganesan Kanchana
International Journal of Research in Ayurveda and Pharmacy , 2011,
Abstract: This study evaluates the cardioprotective effect of esculetin on isoproterenol (ISO)-induced myocardial infarction (MI) in rats. Rats were pretreated with esculetin (10 and 20 mg/kg) orally for a period of 21 days. After the treatment period ISO (85 mg/kg) was administered subcutaneously to rats at an interval of 24 h for 2 days. ISO-induced rats showed a significant increase in the activities of marker enzymes such as creatine kinase (CK), creatine kinase-MB (CK-MB), aspartate transaminase (AST), alanine transaminase (ALT), and lactate dehydrogenase (LDH) in serum and there by subsequent decrease in the heart, and also ISO-induced rats showed a significant increase in heart weight. A significant decrease in the activity of sodium/potassium dependent adenosine triphosphatase (Na+/K+-ATPase) and increased in the activities of calcium and magnesium dependent adenosine triphosphatase (Ca2+ and Mg2+-ATPase) were observed in the heart of ISO-induced rats. Pretreatment with esculetin positively altered the activities of marker enzymes and the biochemical parameters in ISO-induced rats. Thus, our study shows that esculetin posses cardioprotective effect in ISO-induced MI in rats. Results obtained from histopathological studies also supported that esculetin has preventive effect against ISO-induced myocardial infarction.
Neuroprotective Effects of Sodium Ferulate and Its Antidepressant-Like Effect Measured by Acute and Chronic Experimental Methods in Animal Models of Depression  [PDF]
Yongping Zhang, Lijian Yu, Yanping Wang, Mingneng Liao, Xia Zhang, Rundi Ma, Xiaoyu Zhang, Tingxi Yu
Journal of Behavioral and Brain Science (JBBS) , 2011, DOI: 10.4236/jbbs.2011.12006
Abstract: Antidepressants with novel targets and without side effects are in great demand. Ferulic acid (FA) is a ubiquitous phenolic acid of low toxicity, and sodium ferulate (SF) is its sodium salt. Our previous studies have revealed that FA and SF show significant protective effect on excitotoxicity, we now test its potential neuroprotective and antidepressant-like effects. MTT assay and morphological analysis by fluorescence microscopy were adopted to measure the neuroprotective effects of SF; forced-swimming, tail-suspension, and chronic mild stress (CMS) tests were performed to assess its antidepressant-like activity. The results showed that SF had protection against H2O2-induced oxidative damage and dexamethasone (DXM)-induced neurotoxicity pheochromocytoma (PC12) cells. Acute administration of SF markedly decreased the duration of immobility during forced-swimming in rats and mice and tail-supension tests in mice. However, SF has no any effects on reserpine-induced hypothermia, 5-hydroxytryptophan-induced head-twitch response, and potentiation of noradrenaline toxicity in mice. Chronic administration of SF reversed the effects of CMS on consumption of food and sucrose solution, weight gain, and histopathology of hippocampus by light microscopy, and potently shortened the immobility time during forced-swimming test following CMS in rats. This study provides evidence that SF possesses obviously antidepressant-like activity, and the antidepressant-like effect may result from its neuroprotective effects.
Cardioprotective Effect of Paeonol and Danshensu Combination on Isoproterenol-Induced Myocardial Injury in Rats  [PDF]
Hua Li, Yan-Hua Xie, Qian Yang, Si-Wang Wang, Bang-Le Zhang, Jian-Bo Wang, Wei Cao, Lin-Lin Bi, Ji-Yuan Sun, Shan Miao, Jing Hu, Xuan-Xuan Zhou, Peng-Cheng Qiu
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0048872
Abstract: Background Traditional Chinese medicinal herbs Cortex Moutan and Radix Salviae Milthiorrhizaeare are prescribed together for their putative cardioprotective effects in clinical practice. However, the rationale of the combined use remains unclear. The present study was designed to investigate the cardioprotective effects of paeonol and danshensu (representative active ingredient of Cortex Moutan and Radix Salviae Milthiorrhizae, respectively) on isoproterenol-induced myocardial infarction in rats and its underlying mechanisms. Methodology Paeonol (80 mg kg?1) and danshensu (160 mg kg?1) were administered orally to Sprague Dawley rats in individual or in combination for 21 days. At the end of this period, rats were administered isoproterenol (85 mg kg?1) subcutaneously to induce myocardial injury. After induction, rats were anaesthetized with pentobarbital sodium (35 mg kg?1) to record electrocardiogram, then sacrificed and biochemical assays of the heart tissues were performed. Principal Findings Induction of rats with isoproterenol resulted in a marked (P<0.001) elevation in ST-segment, infarct size, level of serum marker enzymes (CK-MB, LDH, AST and ALT), cTnI, TBARS, protein expression of Bax and Caspase-3 and a significant decrease in the activities of endogenous antioxidants (SOD, CAT, GPx, GR, and GST) and protein expression of Bcl-2. Pretreatment with paeonol and danshensu combination showed a significant (P<0.001) decrease in ST-segment elevation, infarct size, cTnI, TBARS, protein expression of Bax and Caspase-3 and a significant increase in the activities of endogenous antioxidants and protein expression of Bcl-2 and Nrf2 when compared with individual treated groups. Conclusions/Significance This study demonstrates the cardioprotective effect of paeonol and danshensu combination on isoproterenol-induced myocardial infarction in rats. The mechanism might be associated with the enhancement of antioxidant defense system through activating of Nrf2 signaling and anti-apoptosis through regulating Bax, Bcl-2 and Caspase-3. It could provide experimental evidence to support the rationality of combinatorial use of traditional Chinese medicine in clinical practice.
Possible involvement of caveolin in attenuation of cardioprotective effect of ischemic preconditioning in diabetic rat heart
Preeti Ajmani, Harlokesh N Yadav, Manjeet Singh, Pyare L Sharma
BMC Cardiovascular Disorders , 2011, DOI: 10.1186/1471-2261-11-43
Abstract: Experimental DM was induced by single dose of streptozotocin (50 mg/Kg, i.p,) and animals were used for experiments four weeks later. Isolated heart was mounted on Langendorff's apparatus, and was subjected to 30 min of global ischemia and 120 min of reperfusion. IPC was given by four cycles of 5 min of ischemia and 5 min of reperfusion with Kreb's-Henseleit solution (K-H). Extent of injury was measured in terms of infarct size by triphenyltetrazolium chloride (TTC) staining, and release of lactate dehydrogenase (LDH) and creatin kinase-MB (CK-MB) in coronary effluent. The cardiac release of NO was noted by measuring the level of nitrite in coronary effluent.IPC- induced cardioprotection and release of NO was significantly decreased in diabetic rat heart. Pre-treatment of diabetic rat with daidzein (DDZ) a caveolin inhibitor (0.2 mg/Kg/s.c), for one week, significantly increased the release of NO and restored the attenuated cardioprotective effect of IPC. Also perfusion of sodium nitrite (10 μM/L), a precursor of NO, significantly restored the lost effect of IPC, similar to daidzein in diabetic rat. Administration of 5-hydroxy deaconate (5-HD), a mito KATP channel blocker, significantly abolished the observed IPC-induced cardioprotection in normal rat or daidzein and sodium nitrite perfused diabetic rat heart alone or in combination.Thus, it is suggested that attenuation of the cardioprotection in diabetic heart may be due to decrease the IPC mediated release of NO in the diabetic myocardium, which may be due to up -regulation of caveolin and subsequently decreased activity of eNOS.Ischemic heart disease is a leading cause of morbidity and mortality worldwide [1]. Reperfusion of an ischemic myocardium is a requisite, for the restoration of the normal functioning of the myocardium [2]. However, abrupt reperfusion of an ischemic myocardium is not without hazard; it produces further damage of myocardium, described as ischemia-reperfusion (I/R) injury [3,4]. Moreover, i
EVALUATION OF CARDIOPROTECTIVE ACTIVITY OF MEDOHAR VATI BY ISOPROTERENOL INDUCED MYOCARDIAL DAMAGE IN RATS  [PDF]
Patel Jignasa S,Setty Seema K,Chakraborty Manodeep,Kamath Jagadish V
International Research Journal of Pharmacy , 2012,
Abstract: This study was designed to investigate the cardioprotective activity of poly herbal formulation Medohar vati in isoproterenol (ISO)- induced myocardial necrosis in rats. Animals were treated with Medohar vati (150 and 300 mg/kg for 21 days) and Carvedilol (10mg/kg for 7 days) to the rats treated with ISO (85 mg/kg, sc) on the 22th and 23rd days. The group only treated with ISO demonstrated elevated level of Lactate dehydrogenasa (LDH), Creatine kinase (CK-MB) and CK- NAC in serum which was restored with all the prophylactic treated groups such as Carvedilol and both the doses of Medohar vati. Similarly the abnormal electocardiographic changes like RR and PR interval, QRS duration, QT segment was normalized by Carvedilol and with both the doses of Medohar vati. The results were supported by the histopathological analysis. To conclude Medohar vati was found to be cardioprotective against ISO induced myocardial damage in rats.
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