scholarly journals Echinacoside Protects against 6-Hydroxydopamine-Induced Mitochondrial Dysfunction and Inflammatory Responses in PC12 Cells via Reducing ROS Production

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Yue-Hua Wang ◽  
Zhao-Hong Xuan ◽  
Shuo Tian ◽  
Guan-Hua Du
Keyword(s):  
Mitochondrial Dysfunction ◽  
Pc12 Cells ◽  
Inflammatory Responses ◽  
Neurodegenerative Disorder ◽  
Cell Damage ◽  
Underlying Mechanism ◽  
Ros Production ◽  
Neuroprotective Effects ◽  
Reduction Activity ◽  
6 Hydroxydopamine

Parkinson’s disease (PD) is a neurodegenerative disorder characterized by progressive loss of dopaminergic (DA) neurons at the substantia nigra. Mitochondrial dysfunction and inflammatory responses are involved in the mechanism of cell damage in PD. 6-Hydroxydopamine (6-OHDA), a dopamine analog, specifically damages dopaminergic neurons. Echinacoside (ECH) is a phenylethanoid glycoside isolated from the stems ofCistanche salsa, showing a variety of neuroprotective effects in previous studies. The present study was to investigate its effect against 6-OHDA-induced neurotoxicity and possible mechanisms in PC12 cells. The results showed that 6-OHDA reduced cell viability, decreased oxidation-reduction activity, decreased mitochondrial membrane potential, and induced mitochondria-mediated apoptosis compared with untreated PC12 cells. However, echinacoside treatment significantly attenuated these changes induced by 6-OHDA. In addition, echinacoside also could significantly alleviate the inflammatory responses induced by 6-OHDA. Further research showed that echinacoside could reduce 6-OHDA-induced ROS production in PC12 cells. These results suggest that the underlying mechanism of echinacoside against 6-OHDA-induced neurotoxicity may be involve in attenuating mitochondrial dysfunction and inflammatory responses by reducing ROS production.

Neuroprotective Effects of Extracts from the Radix Curcuma aromatica on H2O2-induced Damage in PC12 Cells

2018 ◽  
Vol 21 (8) ◽  
pp. 571-582 ◽  
Author(s):  
Juxiang Liu ◽  
Lianli Zhang ◽  
Dan Liu ◽  
Baocai Li ◽  
Mi Zhang
Keyword(s):  
Oxidative Stress ◽  
Pc12 Cells ◽  
Caspase 3 ◽  
Cell Damage ◽  
Positive Control ◽  
Neuroprotective Activity ◽  
Antioxidant Enzyme Activities ◽  
Morphologic Change ◽  
Neuroprotective Effects ◽  
Etoh Extract

Aim & Objectives: Curcuminoids are characteristic constituents in Curcuma, displaying obviously neuroprotective activities against oxidative stress. As one of the Traditional Chinese Medicines from Curcuma, the radix of Curcuma aromatica is also rich in those chemicals, but its neuroprotective activity and mechanism remain unknown. The aim of the current study is to evaluate the neuroprotective effects of extracts from the radix of C. aromatica (ECAs) on H2O2-damaged PC12 cells. Material and Methods: The model of oxidative stress damage was established by treatment of 400 µM H2O2 on PC12 to induce cell damage. After the treatment of ECWs for 24 h, the cell viability, LDH, SOD, CAT and GSH were measured to evaluate the neuroprotection of ECAs on that model. The potential action mechanism was studied by measurement of level of ROS, cell apoptosis rate, mitochondrial membrane potential (MMP), morphologic change, the intracellular Ca2+ content (F340/F380) and the expressions of Bcl-2, Bax and Caspase-3. Additionally, the constituents from tested extracts were analyzed by HPLC-DAD-Q-TOF-MS method. Results: Compared with a positive control, Vitamin E, 10 µg/ml of 95% EtOH extract (HCECA) and 75% EtOH extract (MCECA) can markedly increase the rate of cell survival and enhance the antioxidant enzyme activities of SOD, CAT, increase the levels of GSH, decrease LDH release and the level of ROS, attenuate the intracellular Ca2+ overloading, reduce the cell apoptotic rate and stabilize MMP, down-regulate Bcl-2 expression, up-regulate Bax and caspase-3 expression, and improve the change of cell morphology. The chemical analysis showed that diarylheptanoids and sesquiterpenoids are the major chemicals in tested extracts and the former were richer in HCECA and MCECA than others. Conclusions: These findings indicated that the effects of HCECA and MCECA on inhibiting the cells damage induced by H2O2 in PC12 are better than other extracts from the radix of C. aromatica, and the active constituents with neuroprotective effects consisting in those two active extracts are diarylheptanoids.

scholarly journals Callicarpa Nudiflora Extract Exerts Anti-Inflammatory Effect on H. Pylori-Associated Gastritis Through Repression of ROS/NLRP3/Caspase-1/IL-1β Signaling Axis

2021 ◽  
Author(s):  
Lili Li ◽  
Xiaohui Zhu ◽  
Xingxing Chai ◽  
Xiaoyu Chen ◽  
Xiaohua Su ◽  
...  
Keyword(s):  
Cell Damage ◽  
Underlying Mechanism ◽  
Inflammatory Factors ◽  
Inflammasome Activation ◽  
Ros Production ◽  
Gastric Diseases ◽  
Caspase 1 ◽  
Signaling Axis ◽  
H Pylori

Abstract Helicobacter pylori ( H. pylori ) is a major pathogenic factor for the development of gastric diseases including chronic gastritis and gastric cancer. Callicarpa nudiflora (CN), an air-dried leaves extract of Callicarpa nudiflora Hook. & Arn., has been found to exhibit a broad-spectrum antibacterial effect. In our study, we extracted the active ingredient from air-dried leaves of Callicarpa nudiflora, detected the effect of CN against H. pylori -infected GES-1 cells in vitro , and elucidated the underlying mechanism. GES-1 cells were cocultured with HPSS1 at MOI = 100:1 and treated with different concentrations of CN. Results indicated that CN not only significantly decreased cellular lactate dehydrogenase leakage, but also markedly attenuated H. pylori -induced cell apoptosis and ROS production in GSE-1 cells, therefore protecting gastric epithelial cells against injuries caused by H. pylori . CN also inhibited the secretions of inflammatory factors, such as tumor necrosis factor-α (TNF-α), IL-1β, IL-6 and IL-8. Furthermore, CN remarkably decreased the expression levels of NLRP3, PYCARD, active Caspase-1. In conclusion, CN exhibited highly efficient protective effect against H. pylori -induced gastritis and cell damage; Mechanismly, CN suppressed H. pylori -triggered inflammatory response and pyroptosis through depressing ROS production and NLRP3 inflammasome activation via ROS/NLRP3/IL-1β signaling axis.

scholarly journals Amelioration of Mitochondrial Quality Control and Proteostasis by Natural Compounds in Parkinson’s Disease Models

2019 ◽  
Vol 20 (20) ◽  
pp. 5208 ◽  
Author(s):  
Bongki Cho ◽  
Taeyun Kim ◽  
Yu-Jin Huh ◽  
Jaemin Lee ◽  
Yun-Il Lee
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Mitochondrial Dysfunction ◽  
Neurodegenerative Disorder ◽  
Ubiquitin Proteasome System ◽  
Natural Compounds ◽  
Cellular Damage ◽  
Pathophysiological Mechanism ◽  
Neuroprotective Effects ◽  
Age Related

Parkinson’s disease (PD) is a well-known age-related neurodegenerative disorder associated with longer lifespans and rapidly aging populations. The pathophysiological mechanism is a complex progress involving cellular damage such as mitochondrial dysfunction and protein homeostasis. Age-mediated degenerative neurological disorders can reduce the quality of life and also impose economic burdens. Currently, the common treatment is replacement with levodopa to address low dopamine levels; however, this does not halt the progression of PD and is associated with adverse effects, including dyskinesis. In addition, elderly patients can react negatively to treatment with synthetic neuroprotection agents. Recently, natural compounds such as phytochemicals with fewer side effects have been reported as candidate treatments of age-related neurodegenerative diseases. This review focuses on mitochondrial dysfunction, oxidative stress, hormesis, proteostasis, the ubiquitin‒proteasome system, and autophagy (mitophagy) to explain the neuroprotective effects of using natural products as a therapeutic strategy. We also summarize the efforts to use natural extracts to develop novel pharmacological candidates for treatment of age-related PD.

scholarly journals Natural compounds attenuate heavy metal-induced PC12 cell damage

2020 ◽  
Vol 48 (6) ◽  
pp. 030006052093084
Author(s):  
Lina Yang ◽  
Keshu Shen ◽  
Dongping Ji
Keyword(s):  
Heavy Metal ◽  
Pc12 Cells ◽  
Pc12 Cell ◽  
Therapeutic Potential ◽  
Cell Damage ◽  
Mitochondrial Protein ◽  
Natural Compounds ◽  
Alpha Tocopherol ◽  
Neuroprotective Effects

Objectives To investigate the neuroprotective effects of six natural compounds (caffeine, gallic acid, resveratrol, epigallocatechin gallate [EGCG], L-ascorbic acid and alpha tocopherol [Vitamin E] on heavy metal-induced cell damage in rat PC12 cells. Methods In this in vitro experiment, rat PC12 cells were exposed to four heavy metals (CdCl2, HgCl2, CoCl2 and PbCl2) at different concentrations and cell apoptosis, necrosis and oxidative stress were assessed with and without the addition of the six natural compounds. Results The metals decreased cell viability but the natural compounds attenuated their effects on apoptosis, necrosis and reactive oxygen species (ROS) levels. Mitochondrial protein changes were involved in the regulation. Conclusion Overall, the natural compounds did provide protection against the metal-induced PC12 cell damage. These data suggest that natural compounds may have therapeutic potential against metal-induced neurodegenerative disease.

scholarly journals Erratum: Neuroprotective Effects of Dammarane-Type Saponins from Panax notoginseng on Glutamate-Induced Cell Damage in PC12 Cells

Planta Medica ◽  
2019 ◽  
Vol 85 (09/10) ◽  
pp. e2-e2
Author(s):  
Bao-Bao Zhang ◽  
Xiao-Long Hu ◽  
Yu-Yan Wang ◽  
Jun-Yan Li ◽  
Thi-Anh Pham ◽  
...  
Keyword(s):  
Pc12 Cells ◽  
Cell Damage ◽  
Panax Notoginseng ◽  
Neuroprotective Effects

scholarly journals Nampt/PBEF/visfatin protects PC12 against high glucose-induced neurotoxicity in an in vitro model of diabetic neuropathy via inhibiting oxidative stress, autophagy and apoptosis

2021 ◽  
pp. 1-22
Author(s):  
Sarvin Jahanbani ◽  
◽  
Mehdi Khaksari ◽  
Fatemeh Sadat Bitaraf ◽  
Majid Rahmati ◽  
...  
Keyword(s):  
Diabetic Neuropathy ◽  
Pc12 Cells ◽  
High Glucose ◽  
Mrna Level ◽  
Ros Production ◽  
Neuroprotective Effects ◽  
Autophagy Pathway ◽  
Cellular Pathways ◽  
Vitro Model

Diabetic neuropathy is a well-known complication of diabetes. It has been recently confirmed that hyperglycemia-induced toxicity participates in multiple cellular pathways that are typical for neural deterioration. Nampt/PBEF/visfatin is a novel endogenous ligand, which some studies have shown its neuroprotective effects on neurodegenerative disease. Therefore, we hypothesized that visfatin might prevent high glucose (HG)-induced neurotoxicity via the inhibition of apoptosis, autophagy, and reactive oxygen species (ROS) responses properly. In this study, Pheochromocytoma Cell Line 12 (PC12) cells were exposed to both HG concentrations (50, 75, 100,125, 150 mM) and visfatin (50, 100, 150 ng/ml) in different time-points to determine the optimum time and dose of glucose and visfatin. To investigate the effects of visfatin on HG-induced damage in PC12 diabetic neuropathy model, we examined ROS response, apoptosis, and autophagy by using ROS detection kit, flow cytometry, and Real-time PCR/western blot, respectively. We determined that HG concentration significantly increased ROS level and apoptosis of diabetic PC12 cells. However, visfatin treatment significantly decreased ROS production (P < 0.05) and apoptosis of diabetic PC12 cells (P < 0.0001). Beclin-1 mRNA level (P < 0.05) and Lc3-II protein level (P < 0.05) showed that autophagy pathway is impaired by HG concentrations. We concluded that visfatin could sufficiently decrease neural damage caused by ROS production and apoptosis under HG-induced toxicity.

scholarly journals Protective effect of CoQ10 and Artemisia sieberi combination on PC12 cells model of 6-hydroxydopamine induced toxicity

2020 ◽  
Vol 24 (4) ◽  
pp. 257-267
Author(s):  
Seyed Behnamedin Jameie ◽  
◽  
Mona Farhadi ◽  
Kamelia Gharibzad ◽  
◽  
...  
Keyword(s):  
Pc12 Cells ◽  
Antioxidant Properties ◽  
Combination Method ◽  
Ros Generation ◽  
Therapeutic Effects ◽  
Neuroprotective Effects ◽  
P53 Expression ◽  
Artemisia Sieberi ◽  
Hoechst Staining ◽  
6 Hydroxydopamine

Introduction: Parkinson's disease (PD) is a progressive neurodegenerative disease that affects motor function. The etiology of PD is unknown and routine therapies temporarily relieve the symptoms. Neuroprotective based therapies preserve the remaining neurons and prevent the progression of PD. Artemisia sieberi has anti-cancer and neuroprotective effects. The CoQ10 also is an antioxidant that has proven anti-inflammatory and antioxidant properties. In order to study the effect of Artemisia and CoQ10 on the PD cellular model, the present research was designed. Methods: PC12 cells were treated with different concentrations of 6-hydroxydopamine. Then the cells divided into the control (cells were not treated), DMSO group and experimental groups treated with the different concentrations of Artemisia sieberi extracts, CoQ10 and combination of them for 24h. The viability of the cells, reactive oxygen species (ROS) generation and p53 expression were evaluated. Results: Artemisia at a concentration of 200μg/ml and CoQ10 at a concentration of 75μg/ml significantly increased cell viability in the treated groups after 24h. Their combination showed better and more significant results compared to each alone. Hoechst staining showed significantly reduced apoptosis in treated cells. ROS generation reduced in the treated groups with better results for the combination-treated groups. The same results acquired for the expression of P53 in the treated cells. Conclusion: Regarding the results of both Artemisia and CoQ10, it could be concluded that they act synergistically with possible similar pathways. Although the Artemisia itself showed significant results, it seems that the combination method might have more therapeutic effects.

scholarly journals Cortex Fraxini (Qingpi) Protects Rat Pheochromocytoma Cells against 6-Hydroxydopamine-Induced Apoptosis

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Jing-Jie Li ◽  
Shi-Ya Zhou ◽  
Huan Zhang ◽  
Kim-Hung Lam ◽  
Simon Ming-Yuen Lee ◽  
...  
Keyword(s):  
Neurodegenerative Diseases ◽  
Pc12 Cells ◽  
Neurodegenerative Disorder ◽  
Antioxidant Properties ◽  
Radical Scavenging ◽  
Water Extract ◽  
Total Phenolic ◽  
Potential Candidate ◽  
Induced Apoptosis ◽  
6 Hydroxydopamine

Parkinson’s disease (PD) is a chronic neurodegenerative disorder having close relationship with oxidative stress induced by reactive oxygen species (ROS). Cortex Fraxini (QP) is a kind of traditional Chinese medicinal herb with antioxidant properties. It may be a potential candidate for preventing the development of chronic neurodegenerative diseases. Thus, the key objective of the current study was to investigate the neuroprotective effect of QP water extract on 6-hydroxydopamine (6-OHDA) induced apoptosis in rat pheochromocytoma (PC12) cells. It was found that QP water extract possesses strong antioxidant property with SC50= 0.15 mg/mL. Total phenolic content of QP water extract was found to be 200.78 ± 2.65 mg GAE/g. QP water extract’s free radical scavenging capacity was demonstrated by reversing the increased level of intracellular ROS induced by 6-OHDA, using 2′,7′-dichlorodihydrofluorescein diacetate. Moreover, QP water extract (0.5 mg/mL) could remarkably increase the viability of PC12 cells treated with 6-OHDA. The protective effect of QP water extract was found to be via inhibiting MEK/ERK pathway and reversing PI3-K/Akt/GSK3βpathway. The current results suggest that QP might be a potential candidate for preventing the development of neurodegenerative diseases, such as PD.

scholarly journals Curcumin protects rat hippocampal neurons against pseudorabies virus by regulating the BDNF/TrkB pathway

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Bingjie Yang ◽  
Guodong Luo ◽  
Chen Zhang ◽  
Luqiu Feng ◽  
Xianmei Luo ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Hippocampal Neurons ◽  
Pseudorabies Virus ◽  
Underlying Mechanism ◽  
Protective Effects ◽  
Apoptotic Pathway ◽  
Neuroprotective Effects ◽  
Tropomyosin Related Kinase B ◽  
Underlying Mechanisms ◽  
Oxide Synthase

AbstractPseudorabies virus (PRV) infection can elicit nervous system disorders. Curcumin has been reported to have neuroprotective effects. However, whether curcumin can protect neurons against PRV infection and the underlying mechanisms remain unclear. In the present study, for the first time, the protective effects of curcumin against PRV-induced oxidative stress, apoptosis, and mitochondrial dysfunction in rat hippocampal neurons and the brain-derived neurotrophic factor (BDNF)/tropomyosin-related kinase B (TrkB) pathway were investigated. Results indicated that PRV with a titer of 3.06 × 106 TCID50 (50% tissue culture infective dose) induced oxidative damage of hippocampal neurons 2 h post-infection and that 10 μM curcumin improved the viability of PRV-infected hippocampal neurons. Blocking the BDNF/TrkB pathway reversed the neuroprotective effects of curcumin, which were imparted by decreasing the PRV-induced upregulation of nitric oxide synthase expression, repressing the PRV-activated mitochondrial apoptotic pathway, and mitochondrial dysfunction. To conclude, curcumin exhibited a neuroprotective role against PRV infection by upregulating the BDNF/TrkB pathway. This study provides insight into the anti-PRV neuroprotective application of curcumin and the underlying mechanism in the prophylaxis and treatment of neurological disorders caused by PRV infection.

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