scholarly journals Two Birds One Stone: The Neuroprotective Effect of Antidiabetic Agents on Parkinson Disease—Focus on Sodium-Glucose Cotransporter 2 (SGLT2) Inhibitors

Antioxidants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1935
Author(s):  
Kai-Jung Lin ◽  
Tzu-Jou Wang ◽  
Shang-Der Chen ◽  
Kai-Lieh Lin ◽  
Chia-Wei Liou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neuroprotective Effect ◽  
Incidence Rates ◽  
Experimental Models ◽  
Sglt2 Inhibitors ◽  
Clinical Severity ◽  
Neuroprotective Effects ◽  
Antidiabetic Agents ◽  
Dipeptidyl Peptidase 4 ◽  
Sodium Glucose Cotransporter

Parkinson’s disease (PD) is the second most common neurodegenerative disease after Alzheimer’s disease affecting more than 1% of the population over 65 years old. The etiology of the disease is unknown and there are only symptomatic managements available with no known disease-modifying treatment. Aging, genes, and environmental factors contribute to PD development and key players involved in the pathophysiology of the disease include oxidative stress, mitochondrial dysfunction, autophagic–lysosomal imbalance, and neuroinflammation. Recent epidemiology studies have shown that type-2 diabetes (T2DM) not only increased the risk for PD, but also is associated with PD clinical severity. A higher rate of insulin resistance has been reported in PD patients and is suggested to be a pathologic driver in this disease. Oral diabetic drugs including sodium-glucose cotransporter 2 (SGLT2) inhibitors, glucagon-like peptide-1 (GLP-1) receptor agonists, and dipeptidyl peptidase-4 (DPP-4) inhibitors have been shown to provide neuroprotective effects in both PD patients and experimental models; additionally, antidiabetic drugs have been demonstrated to lower incidence rates of PD in DM patients. Among these, the most recently developed drugs, SGLT2 inhibitors may provide neuroprotective effects through improving mitochondrial function and antioxidative effects. In this article, we will discuss the involvement of mitochondrial-related oxidative stress in the development of PD and potential benefits provided by antidiabetic agents especially focusing on sglt2 inhibitors.

scholarly journals Perspectives of Antidiabetic Drugs in Diabetes With Coronavirus Infections

2021 ◽  
Vol 11 ◽  
Author(s):  
Bao Sun ◽  
Shiqiong Huang ◽  
Jiecan Zhou
Keyword(s):  
Viral Infections ◽  
Sglt2 Inhibitors ◽  
The Novel ◽  
Antidiabetic Agents ◽  
Dipeptidyl Peptidase 4 ◽  
Sodium Glucose Cotransporter ◽  
Coronavirus Infection ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Diabetes mellitus (DM) increases the risk of viral infections especially during the period of poor glycemic controls. Emerging evidence has reported that DM is one of the most common comorbidities in the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) infection, also referred to as COVID-19. Moreover, the management and therapy are complex for individuals with diabetes who are acutely unwell with suspected or confirmed COVID-19. Here, we review the role of antidiabetic agents, mainly including insulin, metformin, pioglitazone, dipeptidyl peptidase-4 (DPP4) inhibitors, sodium-glucose cotransporter 2 (SGLT2) inhibitors, and glucagon-like peptide 1 (GLP-1) receptor agonists in DM patients with coronavirus infection, addressing the clinical therapeutic choices for these subjects.

scholarly journals Neurotherapeutic Effect of Inula britannica var. Chinensis against H2O2-Induced Oxidative Stress and Mitochondrial Dysfunction in Cortical Neurons

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 375
Author(s):  
Jin Young Hong ◽  
Hyunseong Kim ◽  
Junseon Lee ◽  
Wan-Jin Jeon ◽  
Seung Ho Baek ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Cortical Neurons ◽  
Inflammatory Diseases ◽  
Neuroprotective Effect ◽  
Neuroprotective Effects ◽  
Neuronal Viability ◽  
Inula Britannica ◽  
Oxidative Effects

Inula britannica var. chinensis (IBC) has been used as a traditional medicinal herb to treat inflammatory diseases. Although its anti-inflammatory and anti-oxidative effects have been reported, whether IBC exerts neuroprotective effects and the related mechanisms in cortical neurons remain unknown. In this study, we investigated the effects of different concentrations of IBC extract (5, 10, and 20 µg/mL) on cortical neurons using a hydrogen peroxide (H2O2)-induced injury model. Our results demonstrate that IBC can effectively enhance neuronal viability under in vitro-modeled reaction oxygen species (ROS)-generating conditions by inhibiting mitochondrial ROS production and increasing adenosine triphosphate level in H2O2-treated neurons. Additionally, we confirmed that neuronal death was attenuated by improving the mitochondrial membrane potential status and regulating the expression of cytochrome c, a protein related to cell death. Furthermore, IBC increased the expression of brain-derived neurotrophic factor and nerve growth factor. Furthermore, IBC inhibited the loss and induced the production of synaptophysin, a major synaptic vesicle protein. This study is the first to demonstrate that IBC exerts its neuroprotective effect by reducing mitochondria-associated oxidative stress and improving mitochondrial dysfunction.

scholarly journals Artemisinin attenuated oxidative stress and apoptosis by inhibiting autophagy in MPP+-treated SH-SY5Y cells

2021 ◽  
Vol 28 (1) ◽  
Author(s):  
Junqiang Yan ◽  
Hongxia Ma ◽  
Xiaoyi Lai ◽  
Jiannan Wu ◽  
Anran Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Membrane Potential ◽  
Protein Expression ◽  
Mitochondrial Membrane Potential ◽  
Western Blotting ◽  
Cell Apoptosis ◽  
Mitochondrial Membrane ◽  
Caspase 3 ◽  
Neuroprotective Effect ◽  
Neuroprotective Effects

Abstract Background Parkinson’s disease (PD) is the second most common neurodegenerative disease after Alzheimer's disease. The oxidative stress is an important component of the pathogenesis of PD. Artemisinin (ART) has antioxidant and neuroprotective effects. The purpose of this study is to explore the neuroprotective effect of ART on 1-methyl-4-phenyliodine iodide (MPP +)-treated SH-SY5Y cells and underlying mechanism. Methods We used MPP+-treated SH-SY5Y cells to study the neuroprotective effect of ART. Cell viability was measured by MTT assay after incubating the cells with MPP+ and/or ART for 24 h. DCFH-DA was used to detect the level of intracellular reactive oxygen species (ROS), and WST-8 was used to detect the level of superoxide dismutase (SOD). The level of intracellular reduced glutathione (GSH) was detected with 5,5΄-dithiobis-(2-nitrobenzoic acid), and the level of malondialdehyde (MDA) was assessed based on the reaction of MDA and thiobarbituric acid. A mitochondrial membrane potential detection kit (JC-1) was used to detect changes in the mitochondrial membrane potential (MMP), and an Annexin V-FITC cell apoptosis kit was used to detect cell apoptosis. The expression levels of caspase-3, cleaved caspase-3 and the autophagy-related proteins LC3, beclin-1, and p62 were detected by Western blotting. In addition, to verify the change in autophagy, we used immunofluorescence to detect the expression of LC3 and p62. Results No significant cytotoxicity was observed at ART concentrations up to 40 μM. ART could significantly increase the viability of SH-SY5Y cells treated with MPP+ and reduce oxidative stress damage and apoptosis. In addition, the Western blotting and immunofluorescence results showed that MPP+ treatment could increase the protein expression of beclin1 and LC3II/LC3I and decrease the protein expression of p62, indicating that MPP+ treatment could induce autophagy. Simultaneous treatment with ART and MPP+ could decrease the protein expression of beclin1 and LC3II/LC3I and increase the protein expression of p62, indicating that ART could decrease the level of autophagy induced by MPP+. Conclusion Our results indicate that ART has a protective effect on MPP+-treated SH-SY5Y cells by the antioxidant, antiapoptotic activities and inhibition of autophagy. Our findings may provide new hope for the prevention and treatment of PD.

scholarly journals Artemisinin Attenuated Oxidative Stress and Apoptosis by Inhibiting Autophagy in MPP+-treated SH-SY5Y Cell 

2020 ◽  
Author(s):  
Junqiang Yan ◽  
Hongxia Ma ◽  
Xiaoyi Lai ◽  
Jiannan Wu ◽  
Anran Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Dopaminergic Neurons ◽  
Artemisia Annua ◽  
Cell Model ◽  
Neuroprotective Effect ◽  
Critical Role ◽  
Neuroprotective Effects ◽  
Pre Treatment

Abstract Background Parkinson's disease (PD) is the second most common neurodegenerative disease after Alzheimer's. The drugs currently used to treat PD cannot inhibit the development of PD, and long-term use produces severe drug resistance and adverse reaction. Artemisinin (ART) is an active ingredient of Artemisia annua and has a neuroprotective effect, but the mechanism is still unclear. This study was designed to investigate the neuroprotective effect of ART in MPP+-treated SH-SY5Y cells. Results There was no significant cytotoxicity when the ART concentration was under. 40μM. The 20μM ART for 24h could increase the cell viability by reducing oxidative stress and cell apoptosis in MPP+-treated SH-SY5Y cell. In addition, immunoblot and immunofluorescence results showed that MPP+ treatment increased the expression of Beclin1, LC3II/LC3I and decreased the expression of P62, while ART can reverse the changes caused by MPP+. Discussion More and more researches reported that ART and its derivates have neuroprotective effects through anti-oxidant and anti-apoptosis. we found that pre-treated cells with 20μM ART for 4h could significantly increase the viability in Parkinson's disease cell model. The oxidative stress and apoptosis were the main reason for the degeneration of dopaminergic neurons, while artemisinin can attenuate oxidative stress and apoptosis in MPP+-lesioned dopaminergic neurons. The levels of autophagy proteins LC3II/I, Beclin1 and P62 also showed that MPP+ increased the autophagy level, and pre-treatment with ART decreased the autophagy level, which may be the pathological mechanism for artemisinin to reduce oxidative stress damage and apoptosis. Conclusions These results indicate that ART exerts a positive effect on MPP+-treated SH-SY5Y cells in terms of anti-oxidative stress and anti-apoptosis. These effects may be related to autophagy. These findings contribute to a better understanding of the critical role of ART in PD treatment.

scholarly journals EVALUATION OF TAURINE’S NEUROPROTECTIVE EFFECTS ON SH-SY5Y CELLS UNDER OXIDATIVE STRESS

2021 ◽  
Author(s):  
Rafaella Carvalho Rossato ◽  
Alessandro Eustaquio Campos Granato ◽  
Jessica Cristina Pinto ◽  
Carlos Dailton Guedes de Oliveira Moraes ◽  
Geisa Nogueira Salles ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Viability ◽  
Cell Morphology ◽  
Neuroprotective Effect ◽  
Study Strategies ◽  
Neuroprotective Effects ◽  
Human Neuroblastoma ◽  
Characteristic Model ◽  
The Face

ABSTRACTAlzheimer’s disease (AD) is a type of dementia that affects millions of people. Although there is no cure, several study strategies seek to elucidate the mechanisms of the disease. Recent studies address the benefits of taurine. Thus, the present study aims to analyze the neuroprotective effect of taurine on human neuroblastoma, using an in vitro experimental model of oxidative stress induced by hydrocortisone in the SH-SY5Y cell line as a characteristic model of AD. The violet crystal assay was used for cell viability and the evaluation of cell morphology was performed by scanning electron microscopy (SEM). After pretreatment with taurine, the SH-SY5Y cell showed an improvement in cell viability in the face of oxidative stress and improved cell morphology. Thus, the treatment presented a neuroprotective effect.GRAPHICAL ABSTRACT

Essential oils in experimental models of neuropsychiatric disorders: A review

2021 ◽  
Vol 19 ◽  
Author(s):  
Luciana Cristina B. Fernandes ◽  
Ianara Mendonça Costa ◽  
Marco Aurelio M. Freire ◽  
Francisca Overlânia V. Lima ◽  
Francisca Idalina Neta ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Systematic Review ◽  
Cerebral Ischemia ◽  
Essential Oils ◽  
Neurological Disorders ◽  
Biological Effects ◽  
Neuroprotective Effect ◽  
Experimental Models ◽  
Sensory Loss ◽  
Cochrane Library

Background: Neural cells undergo functional or sensory loss due to neurological disorders. In addition to environmental or genetic factors, oxidative stress is a major contributor to neurodegeneration. In this context, there has been a growing interest in investigating the effects of essential oils (EOs) in recent years, especially in the treatment of neuropathologies. The chemical and biological effects of EOs have led to important treatment tools for the management of various neurological disorders. Objective: In the present study we performed a systematic review that sought to comprehend the neuroprotective effects of different EOs. Method: This work is a systematic review where an electronic search was performed on PubMed, Science direct, Cochrane Library and SciELO (Scientific Electronic Library Online) databases, covering the last 10 years, using “Essential oil” and “Neuroprotective effect” as reference terms. Results: A total of 9 articles were identified, in which the efficacy of EOs was described in experimental models of anxiety, dementia, oxidative stress, cerebral ischemia, Alzheimer’s disease and oxidative toxicity. Conclusion: EOs from different species of medicinal plants have shown positive responses in neurological disorders such as anxiety, dementia, oxidative stress, cerebral ischemia and oxidative toxicity. Thus, EOs emerges with the potential to be used as alternative agents in the treatment of neurological disorders.

scholarly journals Renal sodium-glucose cotransporter inhibition in the management of type 2 diabetes mellitus

2015 ◽  
Vol 309 (11) ◽  
pp. F889-F900 ◽  
Author(s):  
Muhammad A. Abdul-Ghani ◽  
Luke Norton ◽  
Ralph A. DeFronzo
Keyword(s):  
Type 2 Diabetes ◽  
Sglt2 Inhibitors ◽  
Diabetic Patients ◽  
Renal Tubules ◽  
Type 2 Diabetic Patients ◽  
Antidiabetic Agents ◽  
Sodium Glucose Cotransporter ◽  
The Us ◽  
Established Relationship

Hyperglycemia is the primary factor responsible for the microvascular, and to a lesser extent macrovascular, complications of diabetes. Despite this well-established relationship, approximately half of all type 2 diabetic patients in the US have a hemoglobin A1c (HbA1c) ≥7.0%. This is associated in part with the side effects, i.e., weight gain and hypoglycemia, of currently available antidiabetic agents and in part with the failure to utilize medications that reverse the basic pathophysiological defects present in patients with type 2 diabetes. The kidney has been shown to play a central role in the development of hyperglycemia by excessive production of glucose throughout the sleeping hours and enhanced reabsorption of filtered glucose by the renal tubules secondary to an increase in the threshold at which glucose spills into the urine. Recently, a new class of antidiabetic agents, the sodium-glucose cotransporter 2 (SGLT2) inhibitors, has been developed and approved for the treatment of patients with type 2 diabetes. In this review, we examine their mechanism of action, efficacy, safety, and place in the therapeutic armamentarium. Since the SGLT2 inhibitors have a unique mode of action that differs from all other oral and injectable antidiabetic agents, they can be used at all stages of the disease and in combination with all other antidiabetic medications.

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.

Activation of Nrf2 by costunolide provides neuroprotective effect in PC12 cells

2019 ◽  
Vol 10 (7) ◽  
pp. 4143-4152 ◽  
Author(s):  
Shoujiao Peng ◽  
Yanan Hou ◽  
Juan Yao ◽  
Jianguo Fang
Keyword(s):  
Oxidative Stress ◽  
Transcription Factor ◽  
Sesquiterpene Lactone ◽  
Pc12 Cells ◽  
Neuroprotective Effect ◽  
Neuroprotective Effects ◽  
Inula Helenium ◽  
Activating Transcription Factor

Costunolide (COS), a natural sesquiterpene lactone originally isolated from Inula helenium (Compositae), shows potent neuroprotective effects against oxidative stress-mediated injuries of PC12 cells via activating transcription factor Nrf2.

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