scholarly journals Neuroprotective effects of Lippia javanica (Burm.F.) Spreng. Herbal tea infusion on Lead-induced oxidative brain damage in Wistar rats

2022 ◽  
Vol 22 (1) ◽  
Author(s):  
Zubair Suleman ◽  
Godwill A. Engwa ◽  
Mathulo Shauli ◽  
Hannibal T. Musarurwa ◽  
Ndinashe A. Katuruza ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Wistar Rats ◽  
Neuronal Damage ◽  
Acetylcholinesterase Activity ◽  
Heart Weight ◽  
Herbal Tea ◽  
Neuroprotective Effects ◽  
Tea Infusion ◽  
Bax Protein ◽  
Lippia Javanica

Abstract Background Though Lippia javanica (Burm.f.) Spreng antioxidant activity has been demonstrated, its effect in protecting the brain from lead (Pb)-induced oxidative damage is unknown. This study investigated the effect of L. javanica against Pb-induced oxidative stress, inflammation, apoptosis and acetylcholinesterase activity in rat’s brain. Methods L. javanica herbal tea infusion was prepared, its phytochemical constituent was revealed by liquid chromatography-Mass spectrometer (LC-MS) and was administered simultaneously with Pb. Four groups of male Wistar rats (n = 5/group) were used: control received distilled water; Pb-acetate group received 50 mg Pb/ Kg bodyweight (bw), treatment group received 50 mg Pb/ Kg Pb-acetate + 5 ml/kg bw L. javanica and L. javanica group received 5 ml/Kg bw of L. javanica tea infusion only. After 6 weeks of treatment, oxidative status, acetylcholinesterase activity, inflammation and apoptosis was assessed in brain tissue which was also histologically examined. Results Mean brain and heart weight was reduced (p < 0.05) while liver and spleen weights were increased (p < 0.05) in Pb exposed animals but were prevented by L. juvanica treatment. Treatment with L. javanica increased (p < 0.05) overall brain antioxidant status (glutathione and superoxide dismutase activities) and reduced lipid peroxidation (p < 0.05) compared to the Pb exposed animals. Pro-inflammatory cytokine tumour necrotic factor-alpha, pro-apoptosis Bax protein and anticholinesterase activity were reduced (p < 0.05) in Pb-L. javanica treated animals compared to the Pb exposed group. Histological examination confirmed neuroprotective effects of L. javanica as evidenced by reduced apoptosis/necrosis and inflammation-induced vacuolization and oedema in the hippocampus. The L. javanica treatment alone had no detrimental effects to the rats. LC-MS analysis revealed L. javanica to be rich in phenolics. Conclusions This study demonstrated that L. javanica, rich in phenolics was effective in reducing Pb-induced brain oxidative stress, inflammation, apoptosis, acetylcholinesterase activity and neuronal damage.

scholarly journals Apoptotic Inducement of Neuronal Cells by Aluminium Chloride and the Neuroprotective Effect of Eugenol in Wistar Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-7 ◽  
Author(s):  
Samuel Bolaji Mesole ◽  
Okpanachi Omachonu Alfred ◽  
Uthman Ademola Yusuf ◽  
Lwiindi Lukubi ◽  
Dailesi Ndhlovu
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Wistar Rats ◽  
Caspase 3 ◽  
Anaesthetic Agent ◽  
Neuroprotective Effect ◽  
Aluminium Chloride ◽  
Neuroprotective Effects ◽  
Stress Markers ◽  
Bax Protein

Aluminium is known to accelerate oxidative stress, amyloid beta (Aβ) deposition, and plaque formation in the brain of rats. Objective. The present study is aimed at studying the neuroprotective effects of eugenol following aluminium-induced neurotoxicity on caspase-3, apoptotic proteins (Bcl-2 and Bax), and oxidative stress markers in Wistar rats such as superoxide dismutase (SOD), glutathione peroxidase (GPx), nitric oxide (NO), and assay oxidative stress to mitochondrial DNA (mtDNA) by measuring the levels of 8-hydroxy-2-deoxyguanosine (8-OHdG). Materials and methods. Twenty (20) adult Wistar rats were randomly divided into four (4) groups with five animals in each group. Route of administration was oral throughout the duration of this study and this study lasted for 21 days. Rats were sacrificed 24 hours after administration of the last dose (i.e., day 22) with 0.8 mg/kg ketamine as an anaesthetic agent. Results. Exposure to AlCl3 resulted in a significant (p<0.01) elevation in the levels of nitric oxide and 8-hydroxy-2-deoxyguanosine (8-OHdG), enhanced the activity of caspase-3, increased the level of proapoptotic protein Bax and reduced the levels of antiapoptotic protein Bcl-2, and significantly (p<0.01) reduced the levels of SOD and GPx. However, treatment with eugenol resulted in a significant reduction (p<0.01) in the levels of nitric oxide (NO) and 8-hydroxy-2-deoxyguanosine (8-OHdG) levels, inhibited the activity of caspase-3, increased levels of Bcl-2 and significantly (p<0.05) reduced levels of Bax protein, respectively, and also significantly (p<0.05) increased the levels of SOD and GPx. Our results would hereby suggest that eugenol would provide a therapeutic value against aluminium-induced oxidative stress as related to antioxidant and antiapoptotic activities.

Neuroprotective Effects of the Anthocleista Schweinfurthii Gilg. (Loganiaceae) Stem Bark Extract in Postmenopause-Like Model of Ovariectomized Wistar Rats

2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Ngoungoure Madeleine Chantal ◽  
Dzeufiet Djomeni Paul Désiré ◽  
Bilanda Danielle Caude ◽  
Mengue Ngandena Yolande Sandrine ◽  
Mbolang Nguegang Lohik ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Plant Extract ◽  
Total Protein ◽  
Wistar Rats ◽  
Stem Bark ◽  
Bark Extract ◽  
Estradiol Valerate ◽  
Neuroprotective Effects ◽  
Protein Levels ◽  
Stem Bark Extract

Abstract Background Estrogen deficiency in postmenopausal period causes severe neuroendocrine changes in brain which influences memory and other nervous functions. Anthocleista schweinfurthii is used traditionally to treat female infertility and menopause related symptoms. This study was performed to investigate the potential neuroprotective effects of aqueous extract of Anthocleista schweinfurthii on brain in a postmenopause-like model of ovariectomized Wistar rats. Methods Thirty animals were sham-operated or ovariectomized (Ovx) 84 days after surgery, six groups of five rats each were daily treated orally during 28 days with: distilled water for groups 1 (sham-operated) and 2 (Ovx), estradiol valerate (group 3) and the three doses of extracts {groups 4, 5 and 6 (Ovx)}. Biochemical and histological evaluations focused on brain. Results Compared to sham-operated control, ovariectomy decreased total protein levels in brain (p<0.01) which was increased by plant extract at the dose of 300 mg/kg (p<0.05), underlying its anabolic properties. Ovariectomy significantly decreased magnesium levels in brain (p<0.001). Anthocleista schweinfurthii increased significantly magnesium levels (p<0.01), showing its capacity to act on synaptic conduction. Ovariectomy induced oxidative stress by increasing malondialdehyde levels (p<0.05) and decreasing reduced glutathione levels (p<0.05) in brain. The plant extract exhibited antioxidative activity by reducing malondialdehyde levels and increasing glutathione levels in brain. Damage in brain structure which was caused by ovariectomy disappeared following the treatment. Conclusions Results suggest that Anthocleista schweinfurthii may have neuroprotective effects in Ovx Wistar rats by increasing total protein, magnesium levels and reducing oxidative stress in brain.

scholarly journals The Neuroprotective Effects ofRatanasampilon Oxidative Stress-Mediated Neuronal Damage in Human Neuronal SH-SY5Y Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Aiqin Zhu ◽  
Zhou Wu ◽  
Jie Meng ◽  
Patrick L. McGeer ◽  
Yi Zhu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Dna Damage ◽  
Molecular Mechanisms ◽  
Neuronal Damage ◽  
Mitogen Activated Protein Kinase ◽  
Tibetan Medicine ◽  
Dependent Manner ◽  
Neuroprotective Effects ◽  
Human Neuroblastoma ◽  
Traditional Tibetan Medicine

We previously found thatRatanasampil(RNSP), a traditional Tibetan medicine, improves the cognitive function of mild-to-moderate AD patients living at high altitude, as well as learning and memory in an AD mouse model (Tg2576); however, mechanism underlying the effects of RNSP is unknown. In the present study, we investigated the effects and molecular mechanisms of RNSP on oxidative stress-induced neuronal toxicity using human neuroblastoma SH-SY5Y cells. Pretreatment with RNSP significantly ameliorated the hydrogen peroxide- (H2O2-) induced cytotoxicity of SH-SY5Y cells in a dose-dependent manner (up to 60 μg/mL). Furthermore, RNSP significantly reduced the H2O2-induced upregulation of 8-oxo-2′-deoxyguanosine (8-oxo-dG, the oxidative DNA damage marker) but significantly reversed the expression of repressor element-1 silencing transcription factor (REST) from H2O2associated (100 μM) downregulation. Moreover, RNSP significantly attenuated the H2O2-induced phosphorylation of p38 mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase 1/2 (ERK 1/2) in SH-SY5Y cells. These observations strongly suggest that RNSP may protect the oxidative stress-induced neuronal damage that occurs through the properties of various antioxidants and inhibit the activation of MAPKs. We thus provide the principle molecular mechanisms of the effects of RNSP and indicate its role in the prevention and clinical management of AD.

scholarly journals Icariin Inhibits AGE-Induced Injury in PC12 Cells by Directly Targeting Apoptosis Regulator Bax

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Shao-Yang Zhao ◽  
Li-Xi Liao ◽  
Peng-Fei Tu ◽  
Wei-Wei Li ◽  
Ke-Wu Zeng
Keyword(s):  
Oxidative Stress ◽  
Pc12 Cells ◽  
Pc12 Cell ◽  
Cell Apoptosis ◽  
Diabetic Patients ◽  
Neuroprotective Effects ◽  
Apoptosis Pathway ◽  
Bax Protein ◽  
Pulldown Assay ◽  
And Migration

Diabetic encephalopathy (DE) is a serious complication caused by long-term cognitive impairment in diabetic patients. At present, there is no effective treatment for DE. Icariin (ICA) is a bioactive ingredient isolated from Epimedium. Previous research indicated that ICA was neuroprotective against Aβ-induced PC12 cell insult; however, the effect of ICA on an advanced glycosylation end product- (AGE-) induced neural injury model has not been studied. In this study, we investigated the neuroprotective effects of ICA on AGE-induced injury in PC12 cells. Our findings revealed that ICA could effectively protect PC12 cells from AGE-induced cell apoptosis by suppressing oxidative stress. Moreover, we observed that ICA could significantly protect against mitochondrial depolarization following AGE stimulation and inactivate the mitochondria-dependent caspase-9/3 apoptosis pathway. Most notably, we identified the direct target protein of ICA as apoptosis regulator Bax by a pulldown assay. We found that ICA could specifically target Bax protein and inhibit Bax dimer formation and migration to mitochondria. Furthermore, a siRNA knockdown experiment revealed that ICA could inhibit PC12 cell apoptosis and oxidative stress through targeting Bax. Taken together, our findings demonstrated that ICA could attenuate AGE-induced oxidative stress and mitochondrial apoptosis by specifically targeting Bax and further regulating the biological function of Bax on mitochondria.

Protective Effect of Kaempferol on the Transgenic Drosophila Model of Alzheimer’s Disease

2018 ◽  
Vol 17 (6) ◽  
pp. 421-429 ◽  
Author(s):  
Tanveer Beg ◽  
Smita Jyoti ◽  
Falaq Naz ◽  
Rahul ◽  
Fahad Ali ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Beta ◽  
Neuronal Damage ◽  
Natural Antioxidants ◽  
Acetylcholinesterase Activity ◽  
Model Of Alzheimer’S Disease ◽  
Climbing Ability ◽  
Transgenic Drosophila

Background: Alzheimer’s disease (AD) is characterized by the accumulation and deposition of β-amyloid peptides leading to a progressive neuronal damage and cell loss. Besides several hypotheses for explaining the neurodegenerative mechanisms, oxidative stress has been considered to be one of them. Till date, there is no cure for AD, but the pathogenesis of the disease could be delayed by the use of natural antioxidants. In this context, we decided to study the effect of kaempferol against the transgenic Drosophila expressing human amyloid beta-42. Method: The AD flies were allowed to feed on the diet having 10, 20, 30 and 40µM of kaempferol for 30 days. After 30 days of exposure, the amyloid beta flies were studied for their climbing ability and Aversive Phototaxis Suppression assay. Amyloid beta flies head homogenate was prepared for estimating the oxidative stress markers, Caspase and acetylcholinesterase activity. Results: The results of the present study reveal that the exposure of AD flies to kaempferol delayed the loss of climbing ability, memory, reduced the oxidative stress and acetylcholinesterase activity. Conclusion: Kaempferol could be used as a possible therapeutic agent against the progression of the Alzheimer’s disease.

scholarly journals Riboceine Regimen Attenuates Ethanol-induced Neuronal Damage in the Cerebellum of Adult Male Wistar Rats

2021 ◽  
Vol 15 (4) ◽  
pp. 249-256
Author(s):  
Taiwo Adekemi Abayomi ◽  
◽  
Olorunfemi Samuel Tokunbo ◽  
Moyinoluwa Ajayi ◽  
Olawale Ayobami Abayomi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Wistar Rats ◽  
Neuronal Damage ◽  
Motor Impairment ◽  
Stress Profile ◽  
Stress Markers ◽  
Ethanol Toxicity ◽  
Male Wistar Rats ◽  
Cerebellar Astrocytes ◽  
The Brain

Background: Although ethanol exerts its neurotoxic effect on the brain through inflammatory and oxidative processes, the effect of Riboceine on the brain following ethanol neurotoxicity is yet to be elucidated. Therefore, this study was designed to evaluate the effects of riboceine on the cellular, behavioral, and molecular impairments induced by ethanol toxicity in rats. Methods: A total of 24 male Wistar rats weighing between 160-170 grams were used for the study, and were divided into four groups of six rats each. After completion of the administration of ethanol and riboceine, and testing for motor impairment, the rats were sacrificed. The cerebellum was excised and processed for oxidative stress analyses, based on oxidative stress markers and histological examinations. The immunohistochemical expression of astrocytes in the cerebellum was examined, using Glial Fibrillary Acidic Protein (GFAP) stain. Results: This study demonstrated that ethanol-induced neurotoxicity in the cerebellum, characterized by increased oxidative stress profile, astrocyte activation, and neuronal death in the cerebellum, especially the Purkinje layer. Necrosis, significant decrease in Superoxide Dismutase (SOD), Catalase (CAT) and Gluathione (GSH) activities (P<0.05) as well as astrogliosis was associated with ethanol treatment. However, riboceine was observed to significantly increase the cerebellar SOD, CAT and GSH activities with significantly reduced Malondialdehyde (MDA) levels (P<0.05). It also attenuated the histomorphological alteration of the cerebellum and reduced the cerebellar astrocytes activation following ethanol-induced neurotoxicity, thus leading to the attenuation of motor impairment. Conclusion: Riboceine attenuated motor impairment caused by chronic ethanol-induced neurotoxicity, suggestive of its anti-oxidative and anti-inflammatory properties.

scholarly journals Cerebral cortex damage induced by acute oral alcohol intake is associated with oxidative stress in Wistar rats (Rattus norvegicus)

2018 ◽  
Vol 7 (1) ◽  
pp. 1113-1120
Author(s):  
Eweoya Olugbenga Olawale ◽  
Ayuba Lolo Shunom ◽  
Ajayi Abayomi
Keyword(s):  
Oxidative Stress ◽  
Cerebral Cortex ◽  
Wistar Rats ◽  
Alcohol Intake ◽  
Structural Changes ◽  
Sucrose Solution ◽  
Neuronal Loss ◽  
Acetylcholinesterase Activity ◽  
Alcoholic Solution ◽  
Control Group

The prefrontal cortex undergoes functional and structural changes due to binge or chronic alcohol consumption. This study examines alcohol-induced cerebral cortex damage and the association with oxidative stress in an animal model. Twenty-four Wistar rats (12 males and 12 females) weighing 150g to 250g were divided into four groups, A, B, C and D according to their weights. The rats in groups B, C and D were administered with 2mls of 52.5%, 16.5% and 4.3% v/v aqueous alcoholic solution respectively for 21 days. While rats in group A (control group) were given distilled water only, for the same period. The brain of each rat was excised, weighed and fixed in 10% formal saline for histological analysis while others were immersed in ice cold 30% sucrose solution, homogenized and analyzed for superoxide dismutase, malondialdehyde and acetylcholinesterase activity. Results indicate chromatolysis of Nissl bodies, cortical necrosis, and uneven neuronal loss with varying range of vacuolations in the prefrontal cortices of the alcohol treated rats in a dosedependent manner when compared with the control group. Cerebral cortex damage due to acute oral alcohol intake is associated with oxidative stress.Keywords: Brain, cerebral cortex, alcohol, Wistar rats, oxidative stress

scholarly journals Ginsenoside-Rg1 Rescues Stress-Induced Depression-Like Behaviors via Suppression of Oxidative Stress and Neural Inflammation in Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-15 ◽  
Author(s):  
Ye Li ◽  
Liyan Wang ◽  
Peng Wang ◽  
Cuiqin Fan ◽  
Ping Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Responses ◽  
Therapeutic Potential ◽  
Neuronal Damage ◽  
Present Report ◽  
Mild Stress ◽  
Ginsenoside Rg1 ◽  
Neuroprotective Effects ◽  
Related Condition ◽  
Antioxidant Stress

Depression is an inflammatory-related condition, with the progression in neuronal damage resulting in major depression disorder. Ginsenoside-Rg1, a sterol extract from the herb Panax ginseng, has been shown to exert neuroprotective effects upon neurodegeneration disorders. However, whether ginsenoside-Rg1 confers antidepressant-like effects on neuroinflammation as associated with depression, as well as the possible mechanism involved in these neuroprotective effects, is currently unclear. In the present report, we show that treatment with ginsenoside-Rg1 (40 mg/kg, i.p.) significantly ameliorated depressive-like behaviors as induced by chronic unpredictable mild stress (CUMS) in a rat model of depression. Moreover, these CUMS rats treated with ginsenoside-Rg1 showed reductions in the levels of the oxidative stress products and the activity in the antioxidant stress kinase. Furthermore, CUMS rats treated with ginsenoside-Rg1 showed ameliorated neuroinflammation and associated neuronal apoptosis along with a reduction in dendritic spine atrophy and display of depressive behaviors. Taken together, the results of this study suggest that ginsenoside-Rg1 produces antidepressant-like effects in CUMS-exposed rats; and one of the mechanisms for these antidepressant-like effects of ginsenoside-Rg1 appears to involve protection against oxidative stress and thus the neuronal deterioration resulting from inflammatory responses. These findings provide evidence for the therapeutic potential of ginsenoside-Rg1 in the treatment of stress-related depression.

scholarly journals Insulin-like Growth Factor II Prevents MPP+ and Glucocorticoid Mitochondrial-Oxidative and Neuronal Damage in Dopaminergic Neurons

Antioxidants ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 41
Author(s):  
Silvia Claros ◽  
Pablo Cabrera ◽  
Nadia Valverde ◽  
Silvana Y. Romero-Zerbo ◽  
Manuel Víctor López-González ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Growth Factor ◽  
Dopaminergic Neurons ◽  
Neuronal Damage ◽  
Cell Damage ◽  
Antioxidant Response ◽  
Insulin Like Growth Factor ◽  
Neuroprotective Effects ◽  
Neuronal Markers ◽  
Factor Ii

Stress seems to contribute to Parkinson’s disease (PD) neuropathology, probably by dysregulation of the hypothalamic–pituitary–adrenal axis. Key factors in this pathophysiology are oxidative stress and mitochondrial dysfunction and neuronal glucocorticoid-induced toxicity. The insulin-like growth factor II (IGF-II), a pleiotropic hormone, has shown antioxidant and neuroprotective effects in some neurodegenerative disorders. Our aim was to examine the protective effect of IGF-II on a dopaminergic cellular combined model of PD and mild to moderate stress measuring oxidative stress parameters, mitochondrial and neuronal markers, and signalling pathways. IGF-II counteracts the mitochondrial-oxidative damage produced by the toxic synergistic effect of corticosterone and 1-methyl-4-phenylpyridinium, protecting dopaminergic neurons from death and neurodegeneration. IGF-II promotes PKC activation and nuclear factor (erythroid-derived 2)-like 2 antioxidant response in a glucocorticoid receptor-dependent pathway, preventing oxidative cell damage and maintaining mitochondrial function. Thus, IGF-II is a potential therapeutic tool for treatment and prevention of disease progression in PD patients suffering mild to moderate emotional stress.

scholarly journals Effects of Consumption of Rooibos (Aspalathus linearis) and a Rooibos-Derived Commercial Supplement on Hepatic Tissue Injury bytert-Butyl Hydroperoxide in Wistar Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
B. D. Canda ◽  
O. O. Oguntibeju ◽  
J. L. Marnewick
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Wistar Rats ◽  
Tissue Injury ◽  
Body Weight Gain ◽  
The Body ◽  
Hepatic Tissue ◽  
Herbal Tea ◽  
Butyl Hydroperoxide ◽  
Male Wistar Rats

This study investigated the antioxidative effect of rooibos herbal tea and a rooibos-derived commercial supplement ontert-butyl hydroperoxide- (t-BHP-) induced oxidative stress in the liver. Forty male Wistar rats consumed fermented rooibos, unfermented rooibos, a rooibos-derived commercial supplement, or water for 10 weeks, while oxidative stress was induced during the last 2 weeks via intraperitoneal injection of 30 µmole oft-BHP per 100 g body weight. None of the beverages impaired the body weight gain of the respective animals. Rats consuming the rooibos-derived commercial supplement had the highest (P<0.05) daily total polyphenol intake (169 mg/day) followed by rats consuming the unfermented rooibos (93.4 mg/day) and fermented rooibos (73.1 mg/day). Intake of both the derived supplement and unfermented rooibos restored thet-BHP-induced reduction and increased (P<0.05) the antioxidant capacity status of the liver, while not impacting on lipid peroxidation. The rooibos herbal tea did not affect the hepatic antioxidant enzymes, except fermented rooibos that caused a decrease (P<0.05) in superoxide dismutase activity. This study confirms rooibos herbal tea as good dietary antioxidant sources and, in conjunction with its many other components, offers a significantly enhanced antioxidant status of the liver in an induced oxidative stress situation.

Sign in / Sign up

Export Citation Format

Share Document