Effects of hyperbaric oxygen pretreatment on brain antioxidant capacity in rats with decompression sickness

2021 ◽  
pp. 287-295
Author(s):  
Ya Li ◽  
◽  
Xiaona Xu ◽  
Junxiang Bao Bao ◽  
Wenlan Wang ◽  
...  
Keyword(s):  
Hyperbaric Oxygen ◽  
Decompression Sickness ◽  
Neuroprotective Effect ◽  
Male Rats ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Rat Models ◽  
Metal Elements ◽  
Flame Atomic Absorption ◽  
Brain Tissues

Objective: Decompression sickness (DCS) causes serious brain hypoxic-ischemic injury. This experiment was designed to observe whether hyperbaric oxygen (HBO2) pretreatment played a neuroprotective effect in decompression sickness rat models and to explore the mechanism of protective effects. Methods: Sprague-Dawley (SD) male rats were pretreated with HBO2 and then underwent decompression to establish the DCS rat model. Antioxidant capacities were evaluated by detecting peroxides (GPx), superoxide dismutase (SOD), catalase (CAT) activity and malondialdehyde (MDA) content in brains. The levels of metal elements manganese (Mn), zinc (Zn), iron (Fe) and magnesium (Mg) in brain tissues were assessed by flame atomic absorption spectrometry. Necrosis and apoptosis of neurons were assessed by H-E staining and immunohistochemical staining. Results: HBO2 pretreatment reduced the degree of necrosis and apoptosis in brain tissues of decompression sickness rat models. In addition, HBO2 pretreatment increased GPx, SOD and CAT activities and reduced MDA accumulation. It also increased the content of Mn, Zn, Fe and Mg in brain tissue, which are all related to free radical metabolism. Conclusion: These results suggested that HBO2 pretreatment has protective effects on brain injury of rats with decompression sickness. The mechanism of the protective effects may be related to reducing oxidative damage by affecting metal elements in vivo.

The protective effects of 1,3-butanediol acetoacetate diester on decompression sickness in rats

2021 ◽  
Author(s):  
Kun Zhang ◽  
Haidong Zhang ◽  
Hongjie Yi ◽  
Guoyang Huang ◽  
Xupeng Zhao ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Decompression Sickness ◽  
Bubble Formation ◽  
Antioxidant Properties ◽  
Oxygen Toxicity ◽  
Causative Factor ◽  
Male Rats ◽  
Drug Candidate ◽  
Pharmacokinetic Analysis ◽  
Protective Effects

Inert gas bubbles are widely accepted as the causative factor of decompression sickness (DCS), resulting in gas embolism and systemic inflammatory responses. The anticonvulsive ketone ester 1,3-butanediol acetoacetate diester (BD-AcAc2) was reported to have the characteristics of increasing blood oxygen partial pressure and anti-inflammation, and was thought to have the potential to reduce bubble formation and alleviate the pathological process of DCS. This study aims to investigate the potential protection of BD-AcAc2 against DCS in a rat model. A single dose of BD-AcAc2 was administered orally to adult male rats (5 g/kg body weight), followed by pharmacokinetic analysis or simulated air dives. After decompression, signs of DCS were monitored, and blood was sampled for biochemical measurements. Blood ketosis peaked at 2 h and lasted for more than 4 h.The incidence of DCS was decreased and postponed significantly in rats treated with BD-AcAc2 compared with those treated with saline (P<0.05). Though BD-AcAc2 failed to reduce bubble load (P>0.05), it showed an obvious decreasing trend. BD-AcAc2 significantly increased blood ppO2 and ameliorated oxidative and inflammatory responses, representing by increased plasma MDA, IL-1, IL-6 and TNF-α and decreased glutathione thiol (P<0.05), while blood pH remained unchanged (P>0.05). These results suggest that BD-AcAc2 exerted beneficial effects on DCS rats mainly related to increasing ppO2, anti-inflammatory and antioxidant properties. Together with its capacity for delaying CNS oxygen toxicity seizures, BD-AcAc2 might be an ideal drug candidate for DCS prevention and treatment.

Abstract 173: The Neuroprotective Effect Of JZL184 is Comparable With Therapeutic Hypothermia in a Rat Model of Cardiac Arrest

Circulation ◽  
2019 ◽  
Vol 140 (Suppl_2) ◽  
Author(s):  
Jing Xu ◽  
Guanghui Zheng ◽  
Juntao Hu ◽  
Weiwei Ge ◽  
Jennifer Bradley ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Therapeutic Hypothermia ◽  
Rat Model ◽  
Neuroprotective Effect ◽  
Experimental Studies ◽  
Flow Index ◽  
Protective Effects ◽  
Cerebral Microcirculation ◽  
Sprague Dawley ◽  
Neuroprotective Effects

Introduction: JZL184 is a synthetic monoacylglycerol lipase inhibitor that reduces brain edema, infarct size and alleviates inflammation following cerebral ischemia in experimental studies. In this study, we compared its cerebral protective effects with therapeutic hypothermia following cardiopulmonary resuscitation (CPR) in a rat model. Hypothesis: JZL184 will have similar neuroprotective effects to therapeutic hypothermia after cardiac arrest (CA) by reducing brain and blood brain barrier (BBB) injury and preserving cerebral microcirculation following CPR. Methods: Thirty six male Sprague-Dawley rats weighing between 450-550 g were randomized: 1) control 2) hypothermia 3) JZL184. Ventricular fibrillation was induced and untreated for 6 min for all rats. Resuscitation was attempted with a 4 Joule defibrillation after 8 min of CPR. Immediately following resuscitation, either hypothermia (33+0.5 o C) or JZL184 (16 mg/k, IP) was administered. Cerebral microcirculation, S-100β, NSE and Evan’s Blue (EB) concentrations were analyzed at 6hrs after resuscitation. Results: NSE and S-100β levels were higher in control compared to hypothermia and JZL18 at 6hr post ROSC (p < 0.001) (Fig. 1). Compared with control, there was a significant decrease in brain permeability to EB in Hypothermia and JZL184 after 6hr post ROSC (p<0.001) (Fig. 2). Microvascular flow index (MFI) was reduced in control compared with hypothermia and JZL184 6hr post ROSC (p <0.01). Conclusions: JZL184 administered following resuscitation reduced brain and BBB injury and preserved cerebral microcirculation at 6 hr post arrest to the same extent as hypothermia in a rat model of cardiac arrest.

Exosome derived from mesenchymal stem cells enhance autophagy and inhibit iNOS/TXNIP/NLRP3 inflammasome axis in injured spinal cord

2020 ◽  
Author(s):  
Bin Lv ◽  
Lei Wang ◽  
Anquan Huang ◽  
Tianming Zou ◽  
Jishan Yuan
Keyword(s):  
Nitric Oxide ◽  
Spinal Cord ◽  
Nlrp3 Inflammasome ◽  
Neuroprotective Effect ◽  
Neuronal Cells ◽  
Tissue Loss ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Cord Injury

Abstract Background: Neuroinflammation, autophagy, NLRP3 inflammasome, and microglia polarizationhave been implicated in spinal cord injury (SCI).Moreover, exosomes, a classic nanovesicles secreted by MSCs, may have a neuroprotective effect on transformation of microglia from the M1 state to the M2 phenotype. However, the effect of MSCs derived exosomes on neuroinflammation is still unclear. Here, we investigated the mechanisms of MSCs derived exosomes mediated NLRP3 inflammasome signaling cascades and its protective effects in SCI. Methods:The SCI model was performed by weight-drop impact in adult male Sprague-Dawley (SD) rats. Control andexosome rats were randomly subjecttoexosomeadminister (20 mg/kg) or placebo via intraperitoneal route 1 h after SCI.Autophagy inhibitor(3-MA) was administered intraperitoneally 20 min before experiment.Neurological function was measured by Basso-Beattie-Bresnahan (BBB) scoring and an open-field test.Neuronal death was measured by HE stainingandNisslstaining.Inducible nitric oxide synthase (iNOS) levels were determined using fluorescent probes. The autophagy and TXNIP and its downstream signaling pathways-mediated polarization of macrophages/microglia was assessed by immunohistochemistry. Results:Exosome significantly downregulated intracellular iNOS and inhibited TXNIP, pyrin domain-containing 3 (NLRP3) inflammasome pathway activation by activating autophagy. Additionally, Exosomepromoted expression of autophagy markers, such as LC3A/B and beclin1,and abrogated the expression of p62. Autophagy inhibitor, 3-MA, blockage of autophagy flux abolished the inhibition of apoptosis and iNOS/TXNIP/NLRP3 inflammasome axisafterSCI. Here, we demonstrated that exosomeadministration in spinal cord markedly reduced tissue loss, attenuate pathological morphology of the injuredregion, and promoted tissue recovery. Moreover. our resultshowed that exosome administration alleviated neuronal cells apoptosis, and inhibited nitric oxide release in microglia.The activation of inflammatoryresponse in neuronal cells facilitates interactions of iNOS‐NLRP3 andTXNIP‐NLRP3and inhibited NLRP3 inflammasome where neuronal cells apoptosis was induced.Further, we found that exosome could suppress macrophages/microglia polarized to M1 phenotype in vivo and in vitro.Taken together, exosome administration exerts protective effects in neuronal cells through inhibiting iNOS production, and exosome administration could inhibit iNOS/TXNIP/NLRP3 inflammasome axis via enhancing autophagy and both in vitro and in vivo. Conclusions:These resultsreveal that exosometreatment alleviatedneuroinflammation and mitigates neuronal apoptosis via autophagy-mediate inhibition of the iNOS/TXNIP/NLRP3 inflammasome axis. Our findings suggest that exosome may be a novel therapeutic target for treating SCI.

scholarly journals Reduction of Traumatic Brain Damage by Tspo Ligand Etifoxine

2019 ◽  
Vol 20 (11) ◽  
pp. 2639 ◽  
Author(s):  
Mona Shehadeh ◽  
Eilam Palzur ◽  
Liat Apel ◽  
Jean Francois Soustiel
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neuronal Damage ◽  
Neuroprotective Effect ◽  
Experimental Studies ◽  
Potential Effect ◽  
Translocator Protein ◽  
Male Rats ◽  
Lesion Volume ◽  
Sprague Dawley

Experimental studies have shown that ligands of the 18 kDa translocator protein can reduce neuronal damage induced by traumatic brain injury by protecting mitochondria and preventing metabolic crisis. Etifoxine, an anxiolytic drug and 18 kDa translocator protein ligand, has shown beneficial effects in the models of peripheral nerve neuropathy. The present study investigates the potential effect of etifoxine as a neuroprotective agent in traumatic brain injury (TBI). For this purpose, the effect of etifoxine on lesion volume and modified neurological severity score at 4 weeks was tested in Sprague–Dawley adult male rats submitted to cortical impact contusion. Effects of etifoxine treatment on neuronal survival and apoptosis were also assessed by immune stains in the perilesional area. Etifoxine induced a significant reduction in the lesion volume compared to nontreated animals in a dose-dependent fashion with a similar effect on neurological outcome at four weeks that correlated with enhanced neuron survival and reduced apoptotic activity. These results are consistent with the neuroprotective effect of etifoxine in TBI that may justify further translational research.

scholarly journals Hyperbaric Oxygen Improves Cerebral Ischemia/Reperfusion Injury in Rats Probably via Inhibition of Autophagy Triggered by the Downregulation of Hypoxia-Inducing Factor-1 Alpha

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Cuiting Wang ◽  
Feng Niu ◽  
Ningna Ren ◽  
Xiaokun Wang ◽  
Hequan Zhong ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Hyperbaric Oxygen ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Hypoxia Inducible Factor ◽  
Treatment Method ◽  
Male Rats ◽  
Sprague Dawley ◽  
Mortality And Morbidity ◽  
Bonferroni Test

Ischemic stroke, accompanied with high mortality and morbidity, may produce heavy economic burden to societies and families. Therefore, it is of great significance to explore effective therapies. Hyperbaric oxygen (HBO) is a noninvasive, nondrug treatment method that has been proved able to save ischemic penumbra by improving hypoxia, microcirculation, and metabolism and applied in various ischemic diseases. Herewith, we fully evaluated the effect of HBO on ischemic stroke and investigated its potential mechanism in the rat ischemia/reperfusion(I/R) model. Sixty Sprague-Dawley male rats were randomly divided into three groups—sham group, MCAO group, and MCAO+HBO group. In the latter two groups, the middle cerebral artery occlusion was performed (MCAO) for 2 hours, and then the occlusion was removed in order to establish the ischemic/reperfusion model. Subsequently, HBO was performed immediately after I/R (2 hours per day for 3 days). 72 hours after MCAO, the brain was dissected for our experiment. Finally, the data from three groups were analyzed by one-way analysis of variance (ANOVA) and followed by a Bonferroni test. In this article, we reported that HBO effectively reduced the infarction and edema and improved neurological functions to a certain extent. As shown by western blot analysis, HBO significantly reduced autophagy by regulating autophagy-related proteins (mTOR, p-mTOR, Atg13, LC3B II and LC3B II) in the hippocampus 72 hours after I/R, which was accompanied by inhibiting the expression of hypoxia inducible factor-1α (HIF-1α) in hippocampus. The results suggest that HBO may improve cerebral I/R injury, possibly via inhibiting HIF-1α, the upstream molecule of autophagy, and therefore, subsequently inhibiting autophagy in the rat model of ischemic stroke.

scholarly journals The protective effects of grape seed oil on induced osteoarthritis of the knee in male rat models

2020 ◽  
Vol 15 (1) ◽  
Author(s):  
Nader Tanideh ◽  
Soheil Ashkani-Esfahani ◽  
Farid Sadeghi ◽  
Omid Koohi-Hosseinabadi ◽  
Cambyz Irajie ◽  
...  
Keyword(s):  
Seed Oil ◽  
Joint Space Width ◽  
Sodium Hyaluronate ◽  
Grape Seed ◽  
Male Rats ◽  
Joint Surface ◽  
Male Rat ◽  
Protective Effects ◽  
Rat Models ◽  
Grape Seed Oil

Abstract Background Osteoarthritis (OA), though being treated via various methods and medicines, is still a major healthcare concern mostly due to the increase in diagnosis of these age-related diseases. The present study aimed at investigating the effects of oral and intra articular injection of grape seed oil on OA in male rat models. Methods and materials Seventy male rats were selected and their anterior cruciate ligament was cut to induce OA. They were divided into 7 groups (n = 10): C1, no treatment; C2, receiving 300 mg/day of Piascledine per os (PO); C3, 1 mg sodium hyaluronate intra-articularly in days 1, 7, 14; C4, 1 mg methyl-prednisolone acetate intra-articularly; E1, avocado and grape seed oil combination (2:1, 300 mg/day) PO; E2, 500 mg/day of grape seed oil PO; E3, 200 mg/day grape seed oil intra-articularly. After 10 weeks, the rats were anesthetized and evaluated radiologically and histopathologically. P value ≤ 0.05 was considered as statistically significant. Results All the groups made significant differences with C1 regarding all inspected radiological criteria (P ≤ 0.05). E1 and E3 showed significantly better effects on medial femoral condyle, medial tibial condyle, joint space width, total osteophyte, and OA scores (P ≤ 0.04). Joint surface, matrix, cell distribution, cell population viability, calcification, and subchondral bone in treatment groups had significantly better scores versus C1 (P ≤ 0.04). E1 and E3 had significantly superior results regarding joint surface, cell viability, and calcification (P ≤ 0.04). Conclusions Grape seed oil has protective effects, both in injectable form and PO in combination with avocado, on OA in rats. Further clinical trials are necessary.

Low-dose Sevoflurane Attenuates Cardiopulmonary Bypass (CPB)- induced Postoperative Cognitive Dysfunction (POCD) by Regulating Hippocampus Apoptosis via PI3K/AKT Pathway

2020 ◽  
Vol 17 (3) ◽  
pp. 232-240
Author(s):  
Jianhua Qin ◽  
Qingjun Ma ◽  
Dongmei Ma
Keyword(s):  
Cardiopulmonary Bypass ◽  
Cognitive Dysfunction ◽  
Low Dose ◽  
Postoperative Cognitive Dysfunction ◽  
Signal Pathway ◽  
Male Rats ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Akt Inhibitor

Background: Cardiopulmonary bypass (CPB) caused postoperative cognitive dysfunction (POCD) was characterized by hippocampus apoptosis, which seriously limited the therapeutic efficacy and utilization of CPB in clinic. Recent data indicated that sevoflurane anesthesia might alleviate CPB-induced POCD, however, the underlying mechanisms are still unclear. Methods: In the present study, the in vivo CPB-POCD models were established by using aged Sprague-Dawley (SD) male rats and the in vitro hypoxia/reoxygenation (H/R) models were inducted by using the primary hippocampus neuron (PHN) cells. Results: The results showed that CPB impaired cognitive functions and induced hippocampus apoptosis in rat models, which were alleviated by pre-treating rats with low-dose sevoflurane. In addition, the phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT) signal pathway was inactivated in the hippocampus tissues of CPB-POCD rats, which were rescued by low-dose sevoflurane treatment. Of note, the PI3K/AKT inhibitor (LY294002) abrogated the protective effects of low-dose sevoflurane on CPB-POCD rats. Consistently, the in vitro results showed that H/R treatment induced cell apoptosis and inhibited cell viability in PHN cells, which were attenuated by low-dose sevoflurane. Similarly, LY294002 abrogated the inhibiting effects of low-dose sevoflurane on H/R-induced PHN cell death. Conclusion: Taken together, low-dose sevoflurane attenuated CPB-induced POCD by inhibiting hippocampus apoptosis through activating PI3K/AKT signal pathway.

scholarly journals Antiperoxidative and anti-apoptotic effects of lycopene and ellagic acid on cyclophosphamide-induced testicular lipid peroxidation and apoptosis

2010 ◽  
Vol 22 (4) ◽  
pp. 587 ◽  
Author(s):  
Gaffari Türk ◽  
Ali Osman Çeribaşi ◽  
Fatih Sakin ◽  
Mustafa Sönmez ◽  
Ahmet Ateşşahin
Keyword(s):  
Lipid Peroxidation ◽  
Ellagic Acid ◽  
Combined Treatment ◽  
Sperm Concentration ◽  
Testicular Tissue ◽  
Male Rats ◽  
Control Group ◽  
Apoptotic Cells ◽  
Protective Effects ◽  
Sprague Dawley

The present study was conducted to investigate the possible protective effects of lycopene (LC) and ellagic acid (EA) on cyclophosphamide (CP)-induced testicular and spermatozoal toxicity associated with the oxidative stress and apoptosis in male rats. Forty-eight healthy adult male Sprague-Dawley rats were divided into six groups of eight rats each. The control group was treated with placebo; the LC, EA and CP groups were given LC (10 mg kg–1), EA (2 mg kg–1) and CP (15 mg kg–1), respectively, alone; the CP+LC group was treated with a combination of CP (15 mg kg–1) and LC (10 mg kg–1); and the CP+EA group was treated with a combination of CP (15 mg kg–1) and EA (2 mg kg–1). All treatments were maintained for 8 weeks. At the end of the treatment period, bodyweight and the weight of the reproductive organs, sperm concentration and motility, testicular tissue lipid peroxidation, anti-oxidant enzyme activity and apoptosis (i.e. Bax and Bcl-2 proteins) were determined. Administration of CP resulted in significant decreases in epididymal sperm concentration and motility and significant increases in malondialdehyde levels. Although CP significantly increased the number of Bax-positive (apoptotic) cells, it had no effect on the number of Bcl-2-positive (anti-apoptotic) cells compared with the control group. However, combined treatment of rats with LC or EA in addition to CP prevented the development of CP-induced lipid peroxidation and sperm and testicular damage. In conclusion, CP-induced lipid peroxidation leads to structural and functional damage, as well as apoptosis, in spermatogenic cells of rats. Both LC and EA protect against the development of these detrimental effects.

scholarly journals Centella asiaticaPrevents Increase of Hippocampal Tumor Necrosis Factor-αIndependently of Its Effect on Brain-Derived Neurotrophic Factor in Rat Model of Chronic Stress

2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Mawaddah Ar Rochmah ◽  
Ika Murti Harini ◽  
Dian Eurike Septyaningtrias ◽  
Dwi Cahyani Ratna Sari ◽  
Rina Susilowati
Keyword(s):  
Chronic Stress ◽  
Neuroprotective Effect ◽  
Centella Asiatica ◽  
Sirtuin 1 ◽  
Male Rats ◽  
Enzyme Linked Immunosorbent Assay ◽  
Sprague Dawley ◽  
Bdnf Expression ◽  
Neurotropic Factor ◽  
The Relationship

Centella asiaticaameliorates memory impairment and induces expression of hippocampal brain-derived neurotropic factor (BDNF) in chronically stressed rats. The relationship between the anti-inflammatory effect ofCentella asiaticaon hippocampal BDNF and the involvement of sirtuin-1, a BDNF expression regulator, in neuroprotective mechanisms ofCentella asiaticawarrants an investigation. We investigated the effect ofCentella asiaticaethanolic extracts (CA) on TNF-α, IL-10, and SIRT1 levels and whether these predicted BDNF expression in rat hippocampus after chronic stress. For the experiments, thirty male rats (Sprague Dawley) were divided into six groups: nonstressed-control, stressed-control, nonstressed +CA 300mg/kg/d, stressed +CA 150 mg/kg/d, stressed +CA 300 mg/kg/d, and stressed +CA 600 mg/kg/d. On day 28, rats were sacrificed and hippocampus was dissected out. Hippocampal TNF-α, IL-10, SIRT1, and BDNF were measured by enzyme-linked immunosorbent assay. Hippocampal TNF-αlevel was significantly higher in the stressed-control compared to nonstressed-control groups. Across all stress conditions, rats receiving the highest dose of CA had the lowest mean TNF-αand highest mean BDNF. There were no significant differences in IL-10 and SIRT1 levels between groups. Hippocampal TNF-αdid not predict hippocampal BDNF in a regression analysis. In conclusion, lower TNF-αand higher BDNF in the hippocampus support the hypothesis that these factors independently contribute toCentella asiatica’s neuroprotective effect in chronically stressed rats.

scholarly journals Neuroprotective Properties of Carvacrol Against Cadmium-induced Neurotoxicity in Male Rats

2021 ◽  
Author(s):  
Mustafa Onur Yıldız ◽  
Hamit Çelik ◽  
Cuneyt Caglayan ◽  
Aydın Genç ◽  
Tuba Doğan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Body Weight ◽  
Nitric Oxide Synthase ◽  
Oxidative Dna Damage ◽  
B Cell Lymphoma ◽  
Mitogen Activated Protein Kinase ◽  
Male Rats ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Oxide Synthase

Abstract Cadmium (Cd), is a heavy metal reported to be associated with oxidative stress and inflammation. In this paper, we investigated the possible protective effects of carvacrol (CRV) against Cd-induced neurotoxicity in rats. Adult male Sprague Dawley rats were treated orally with Cd (25 mg/kg body weight) and with CRV (25 and 50 mg/kg body weight) for 1 week. CRV decreased the levels of malondialdehyde (MDA), glial fibrillary acidic protein (GFAP) and monoamine oxidase (MAO), and significantly increased the levels of glutathione (GSH) and activities of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) in brain tissue. Additionally, CRV alleviated the in levels of inflammation and apoptosis related proteins involving p38 mitogen-activated protein kinase (p38 MAPK), cyclooxygenase-2 (COX-2), nuclear factor kappa B (NF-κB), B-cell lymphoma-3 (Bcl-3), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), myeloperoxidase (MPO), prostaglandin E2 (PGE2), neuronal nitric oxide synthase (nNOS), inducible nitric oxide synthase (iNOS), cysteine aspartate specific protease-3 (caspase-3) and Bcl-2 associated X protein (Bax) in the Cd-induced neurotoxicity. CRV also decreased the mRNA expression of matrix metalloproteinases (MMP9 and MMP13), as well as 8-hydroxy-2′-deoxyguanosine (8−OHdG) level, a marker of oxidative DNA damage. Collectively, our findings indicated that CRV has a beneficial effect in ameliorating the Cd-induced neurotoxicity in the brain of rats.

Sign in / Sign up

Export Citation Format

Share Document