scholarly journals Afrostyrax lepidophyllus Mildbr. and Monodora myristica (Gaertn.) Dunal Extracts Decrease Doxorubicin Cytotoxicity on H9c2 Cardiomyoblasts

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Bruno M. Moukette ◽  
José P. Castelão-Baptista ◽  
Luciana Ferreira ◽  
Ana M. Silva ◽  
Rui F. Simões ◽  
...  
Keyword(s):  
Vitamin C ◽  
Plant Extracts ◽  
Superoxide Anion ◽  
Caspase 3 ◽  
Cell Mass ◽  
Antioxidant Properties ◽  
Protective Effects ◽  
Caspase 9 ◽  
H9c2 Cardiomyoblasts ◽  
Monodora Myristica

Ethnopharmacological Relevance. Doxorubicin (Dox) is an anthracycline antibiotic widely used in cancer treatment. Despite its antitumor efficacy, its clinical application is significantly limited because of its cardiotoxicity originated, among other factors, from pro-oxidant damage to cardiac mitochondria. Phytochemicals represent a potentially attractive strategy to mitigate Dox cardiotoxicity due to their antioxidant properties, with plant extracts used in traditional medicine often being ignored in terms of potential therapeutic uses. Aim of the Study. The present study aimed at investigating the protective effects of two native Cameroonian plants, Afrostyrax lepidophyllus Mildbr. (A. lepidophyllus) and Monodora myristica (Gaertn.) Dunal (M. myristica), against Dox-induced cytotoxicity on cultured H9c2 cardiomyoblast cells. Materials and Methods. Bark extracts of these plants (1 and 25 µg/mL) were added 3 hours before coincubating H9c2 cardiomyoblasts with Dox (0.5 and 1 µM) for 24 hours more. We measured cell mass and metabolic viability, mitochondrial transmembrane potential, superoxide anion content, and activity-like of caspase-3 and caspase-9 following treatment with the extracts and/or Dox. Also, selenium and vitamin C contents were measured in the plant extracts. Results. The results confirmed that Dox treatment decreased cell mass, mitochondrial membrane potential and metabolic viability, increased mitochondrial superoxide anion, and stimulated caspase-3 and caspase-9-like activities. Pretreatment of the cells with the plant extracts significantly inhibited Dox cytotoxicity, with more significant results at the higher concentration. Measurements of selenium and vitamin C in the extracts revealed higher concentration of both when compared with other Cameroonian spices. Conclusion. Both extracts of A. lepidophyllus and M. myristica were effective against Dox-induced cytotoxicity, most likely due to their content in antioxidants.

scholarly journals Guaiane-Type Sesquiterpenoids From Dendranthema morifolium (Ramat.) S. Kitam Flowers Protect H9c2 Cardiomyocyte From LPS-Induced Injury

2019 ◽  
Vol 14 (7) ◽  
pp. 1934578X1986417
Author(s):  
Beibei Zhang ◽  
Mengnan Zeng ◽  
Meng Li ◽  
Wenjing Chen ◽  
Benke Li ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Creatine Phosphate ◽  
Cardiomyocyte Apoptosis ◽  
Exocyclic Double Bond ◽  
Enzyme Linked Immunosorbent Assay ◽  
Protective Effects ◽  
Caspase 9 ◽  
Necrosis Factor Alpha ◽  
Thiazolyl Blue Tetrazolium Bromide ◽  
Tnf Α

This study investigated the protective effects of guaiane-type sesquiterpenoids isolated from Dendranthema morifolium (Ramat.) S. Kitam flowers on lipopolysaccharide (LPS)-induced injury in H9c2 cardiomyocyte. Cell viability was determined by thiazolyl blue tetrazolium bromide (MTT). The content of released tumor necrosis factor alpha (TNF- α) and interleukin 6 (IL-6) was evaluated by enzyme-linked immunosorbent assay. The levels of lactate dehydrogenase (LDH) and creatine phosphate kinase (CK) were measured by using commercial available kits. The protein expression levels of pelF2 α, GRP78, Bax, caspase-3, caspase-9, Bcl-2, LC3-II, and p62 were measured by in-cell Western. Flow cytometry was used to detect H9c2 cardiomyocyte apoptosis. Compounds 5, 7, 1, 8, and 2 exhibited the effects of cardioprotection and activity sequence enhancement. The levels of IL-6, TNF- α, LDH, CK, pelF2 α, GRP78, Bax, caspase-3, caspase-9, p62, and H9c2 cardiomyocyte apoptosis were increased in LPS-treated H9c2 cardiomyocyte, while those of Bcl-2 and LC3-II were decreased. These effects could be effectively reversed by compounds 5, 7, 1, 8, and 2. Results demonstrated that the guaiane-type sesquiterpenoids could prevent LPS-induced injury in cardiomyocyte by decreasing endoplasmic reticulum (ER) stress, apoptosis, and autophagy as well as downregulating the inflammatory mediators. In addition, the active groups of guaiane-type sesquiterpenoids might be the angelate at C-8 and the exocyclic double bond at C-11.

scholarly journals Assessment of Antioxidant Properties of Classic Energy Drinks in Comparison with Fruit Energy Drinks

Foods ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 56 ◽  
Author(s):  
Dariusz Nowak ◽  
Michał Gośliński
Keyword(s):  
Vitamin C ◽  
Antioxidant Capacity ◽  
Plant Extracts ◽  
Fruit Juice ◽  
Antioxidant Properties ◽  
Energy Drinks ◽  
Health Issues ◽  
Total Polyphenols ◽  
Natural Pigments ◽  
Total Anthocyanins

Energy drinks (EDs) contain sugar, caffeine, and other bioactive compounds. Recently, new types of EDs, enriched with fruit juices, natural pigments, and plant extracts, have been launched in the market. The objective of this study was to investigate the composition and antioxidant properties of the most popular classic and fruit EDs. The study was carried out including 24 of the most popular energy drinks (classic and fruit EDs). The composition of EDs, especially caffeine and sugar, and antioxidant properties (antioxidant capacity, total polyphenols, total anthocyanins, vitamin C) were analyzed. Energy drinks with added fruit juice or natural pigments had a significantly higher (p ≤ 0.05) antioxidant capacity compared to classic energy drinks. Fruit EDs had a higher concentration of polyphenols and vitamin C. In some fruit EDs, slight amounts of anthocyanins were found. Generally, EDs are not a rich source of polyphenols and are not distinguished by high antioxidant capacity. However, fruit energy drinks and/or ones with added natural pigments have much better antioxidant properties than classic EDs. Both classic and fruit EDs contain a large amount of caffeine and sugar, therefore, it would be advisable not to drink large amounts of EDs for possible related health issues.

scholarly journals Downregulation of Endogenous Hydrogen Sulfide Pathway Is Involved in Mitochondrion-Related Endothelial Cell Apoptosis Induced by High Salt

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Yanfang Zong ◽  
Yaqian Huang ◽  
Siyao Chen ◽  
Mingzhu Zhu ◽  
Qinghua Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Membrane Potential ◽  
Endothelial Cell ◽  
Cell Apoptosis ◽  
Superoxide Anion ◽  
Mitochondrial Membrane ◽  
Caspase 3 ◽  
High Salt ◽  
Caspase 9

Background. The study aimed to investigate whether endogenous H2S pathway was involved in high-salt-stimulated mitochondria-related vascular endothelial cell (VEC) apoptosis.Methods. Cultured human umbilical vein endothelial cells (HUVECs) were used in the study. H2S content in the supernatant was detected. Western blot was used to detect expression of cystathionine gamma-lyase (CSE), cleaved-caspase-3, and mitochondrial and cytosolic cytochrome c (cytc). Fluorescent probes were used to quantitatively detect superoxide anion generation and measure thein situsuperoxide anion generation in HUVEC. Mitochondrial membrane pore opening, mitochondrial membrane potential, and caspase-9 activities were measured. The cell apoptosis was detected by cell death ELISA and TdT-mediated dUTP nick end labeling (TUNEL) methods.Results. High-salt treatment downregulated the endogenous VEC H2S/CSE pathway, in association with increased generation of oxygen free radicals, decreased mitochondrial membrane potential, enhanced the opening of mitochondrial membrane permeability transition pore and leakage of mitochondrial cytc, activated cytoplasmic caspase-9 and caspase-3 and subsequently induced VEC apoptosis. However, supplementation of H2S donor markedly inhibited VEC oxidative stress and mitochondria-related VEC apoptosis induced by high salt.Conclusion. H2S/CSE pathway is an important endogenous defensive system in endothelial cells antagonizing high-salt insult. The protective mechanisms for VEC damage might involve inhibiting oxidative stress and protecting mitochondrial injury.

Propofol Attenuates Peroxynitrite-mediated DNA Damage and Apoptosis in Cultured Astrocytes

2004 ◽  
Vol 101 (6) ◽  
pp. 1363-1371 ◽  
Author(s):  
Rosaria Acquaviva ◽  
Agata Campisi ◽  
Paolo Murabito ◽  
Giuseppina Raciti ◽  
Roberto Avola ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Antioxidant Properties ◽  
Lactic Dehydrogenase ◽  
Protective Effects ◽  
Astroglial Cells ◽  
Experimental Conditions ◽  
Scavenging Effect ◽  
Cultured Astrocytes ◽  
Diphenyl Tetrazolium Bromide

Background The concentration of peroxynitrite in the brain increases after central nervous system injuries. The authors hypothesized that propofol, because of its particular chemical structure, mitigates the effects of peroxynitrite-mediated oxidative stress and apoptosis by the induction of heme oxygenase (HO)-1 in primary cultured astroglial cells. Methods Primary cultured astroglial cells were incubated for 18 h with a known peroxynitrite donor (3 mm SIN-1) in the presence or absence of propofol (40 microm, 80 microm, 160 microm, and 1 mm). The protective effects of propofol were evaluated by 3(4,5-dimethyl-thiazol-2-yl)2,5-diphenyl-tetrazolium bromide cytotoxicity assay, lactic dehydrogenase release, DNA ladderization by Comet assay, and caspase-3 activation by Western blot analysis. Results Appropriate propofol concentrations (ranging from 40 microm to 1 mm) significantly increased HO-1 expression and attenuated SIN-1-mediated DNA ladderization and caspase-3 activation. The protective effects of propofol were mitigated by the addition of tin mesoporphyrin, a potent inhibitor of HO activity. The addition of a specific synthetic inhibitor of nuclear factor kappaB abolished propofol-mediated HO-1 induction, suggesting a possible role of this nuclear transcriptional factor in our experimental conditions. Conclusions The antioxidant properties of propofol can be partially attributed to its scavenging effect on peroxynitrite as well as to its ability to increase HO-1 expression at higher concentrations, a property that might be relevant to neuroprotection during anesthesia.

scholarly journals Ameliorative Effects of Nano-Selenium Against Fluoride Stress Induced Hepatocytes Autophagy and Apoptosis in Mice

2020 ◽  
Author(s):  
Yajing Wang ◽  
Bingxian Liu ◽  
Qingyue Han ◽  
Khalid Mehmood ◽  
Fazul Nabi ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Beclin 1 ◽  
Protective Effects ◽  
Human Beings ◽  
Caspase 9 ◽  
Nano Material ◽  
Cyt C ◽  
Hepatocyte Damage

Abstract Background: Fluorine is widespread in the environment, and the injurious impacts of fluoride underscore its significance for public health. The long-term presence of fluorine in environment could be a risk in hepatotoxicity for both human beings and animals. Important role of selenium in mitigation of heavy metal toxicity via regulating autophagy and apoptosis is well-known. Further, nano-Se is a common artificial nano material, with higher biological activity and lower toxicity. The aim of the current study was to examine whether nano-Se supplementation can reduce the effects of fluoride-induced hepatocytes autophagy and apoptosis. Results: Here, we report that fluoride exposure induces apoptosis and autophagy with nucleus broken, dissolved and disappeared of hepatocyte, contributing to its hepatotoxicity. More importantly, Cyt-C and Beclin-1/Bcl-2 pathways are involved in the regulation of autophagy and apoptosis via targeting Caspase-9, Caspase-3, P53, Bax, LC3, ATG-5, P62 and mTOR expressions. Conclusion: Nano-Se is capable to alleviate fluoride-induced hepatocyte damage, that selenium can be prefer to prevent chronic fluorosis-induced autophagy and apoptosis by regulating Cyt-C and Beclin-1/Bcl-2 signaling pathway. In precisely, NaF-induced the liver injury by activating autophagy and apoptosis, which indicate that fluorine exposure, pose an ecological risk to human beings and animals. Nano-Se has protective effects against fluoride-induced hepatocytes.

scholarly journals Vitamin C Inhibits Aggravated Eryptosis by Hydrogen Peroxide in Glucose-6-Phosphated Dehydrogenase Deficiency

2016 ◽  
Vol 39 (4) ◽  
pp. 1453-1462 ◽  
Author(s):  
Feng Shan ◽  
Rui Yang ◽  
Tiemei Ji ◽  
Fengjun Jiao
Keyword(s):  
Hydrogen Peroxide ◽  
Vitamin C ◽  
G6pd Deficiency ◽  
Caspase 3 ◽  
Annexin V ◽  
Normal Activity ◽  
Protective Effects ◽  
Blank Group ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Active Caspase

Background/Aims: The study was aimed to investigate if vitamin C could exert protective effects on development of eryptosis caused by glucose-6-phosphate dehydrogenase (G6PD) deficiency and hydrogen peroxide. Methods: Isolated erythrocytes with different G6PD activity (normal or deficient) were divided into various groups treated by either Vitamin C or H2O2. Phosphatidylserine (PS) extroversion rate was detected by Annexin V binding. The intracellular Ca2+ concentration was detected by Fluo3-fluorescence, and western blot was used to detect the expression of apoptosis factor caspase 3. Results: Compared with the blank group, the PS extroversion rate (P < 0.001), intracellular Ca2+ concentration (P < 0.001) and active caspase 3 expression level (P < 0.05) of erythrocytes significantly increased after treatment of 0.05% H2O2. Then the index of eryptosis significantly decreased after erythrocytes were treated with Vitamin C (1 mg/ml) for 30 min (all P < 0.05). The decline in erythrocytes with G6PD normal activity was more significant than those with G6PD deficiency. Conclusion: Vitamin C could effectively inhibit the eryptosis contributed by H2O2 oxidative stress, and the suppression on eryptosis with G6PD normal activity was more effective than that with G6PD deficiency.

scholarly journals Phosphocreatine Improves Cardiac Dysfunction by Normalizing Mitochondrial Respiratory Function through JAK2/STAT3 Signaling Pathway In Vivo and In Vitro

2019 ◽  
Vol 2019 ◽  
pp. 1-18 ◽  
Author(s):  
Eskandar Qaed ◽  
Jiaqi Wang ◽  
Marwan Almoiliqy ◽  
Yanlin Song ◽  
Wu Liu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Caspase 3 ◽  
Male Rats ◽  
Protective Effects ◽  
Caspase 9 ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway ◽  
Mitochondrial Respiratory

Diabetic cardiomyopathy (DCM) is one of the common cardiovascular complications in patients with diabetes. Accumulating evidence has demonstrated that DCM is thoroughly related to mitochondrial energy impairment and increases the generation of reactive oxygen species (ROS). Therefore, an ongoing study is developing strategies to protect cardiac mitochondria from diabetic complications, especially from hyperglycemia. Phosphocreatine (PCr) plays a major metabolic role in cardiac muscular cells including intracellular concentration of ATP which affects the activity of the myocardium. We hypothesized that PCr might improve oxidative phosphorylation and electron transport capacity in mitochondria impaired by hyperglycemia in vivo and in vitro. Also, we aimed to evaluate the protective effect of PCr against DCM through the JAK2/STAT3 signaling pathway. The mitochondrial respiratory capacity from rats and H9C2 cells was measured by high-resolution respirometry (HRR). Expressions of proteins Bax, Bcl-2, caspase 3, caspase 9, cleaved caspase 3, and cleaved caspase 9, as well as JAK2/STAT3 signaling pathways, were determined by western blotting. ROS generation and mitochondrial membrane potential (MMP) were measured with fluorescent probes. Type 1 diabetes mellitus was induced in Wistar male rats by a single intraperitoneal injection of streptozotocin (STZ) (80 mg/kg body weight). Our results revealed that PCr possessed protective effects against DCM injury by improving the mitochondrial bioenergetics and by positively exerting protective effects against DCM in vivo and in vitro, not only improving diabetes symptom, resulting in changes of cardiac tissue using hematoxylin and eosin (H&E) stain, but also ameliorating biochemical changes. Moreover, PCr increased Bcl-2, caspase 3, and caspase 9 protein expressions and decreased Bax, cleaved caspase 3, and cleaved caspase 9 expressions as well as the JAK2/STAT3 signaling pathway. In conclusion, PCr improves mitochondrial functions and exerts an antiapoptotic effect in vivo and in vitro exposed to oxidative stress by hyperglycemia through the JAK2/STAT3 signaling pathway. Our findings suggest that PCr medication is a possible therapeutic strategy for cardioprotection.

scholarly journals Protective Effects and Mechanisms of Dendrobium nobile Lindl. Alkaloids on PC12 Cell Damage Induced by Aβ25-35

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Yuan Liu ◽  
Tingting Pi ◽  
Xiaohui Yang ◽  
Jingshan Shi
Keyword(s):  
Oxidative Stress ◽  
Pc12 Cell ◽  
Caspase 3 ◽  
Cell Damage ◽  
Protective Effects ◽  
Related Protein ◽  
Caspase 9 ◽  
Apoptosis Pathway ◽  
Mitochondrial Apoptosis Pathway ◽  
Dendrobium Nobile Lindl

Background. Aβ deposition abnormally in the mitochondria can damage the mitochondrial respiratory chain and activate the mitochondrial-mediated apoptosis pathway, resulting in AD-like symptoms. Objective. To observe the protective effects of Dendrobium nobile Lindl. alkaloids (DNLA) on Aβ25-35-induced oxidative stress and apoptosis in PC12 cells explore its possible protective mechanisms. Methods. PC12 cells were treated with DNLA with different concentrations (0.035 mg/L, 0.3 mg/L, and 3.5 mg/L) for 6 h, followed by administration with Aβ25-35 (10 μM) for 24 h. MTT assay and flow cytometer observe the effect of DNLA on Aβ25-35-induced cytotoxicity and apoptosis of PC12 cell. Based on the mitochondrial apoptosis pathway to study the antiapoptotic effect of DNLA on this model and its relationship with oxidative stress, flow cytometer detected the level of reactive oxygen species (ROS), and ELISA kits were used to detect superoxide dismutase activity (SOD) and glutathione (GSH) content in cells. The JC-1 fluorescent staining observed the effect of DNLA on the mitochondrial membrane potential (MMP) with inverted immunofluorescence microscopy. Western blot was used to detect the levels of mitochondrial apoptosis pathway-related protein and its major downstream proteins Bax, Bcl-2, cleaved-caspase-9, and cleaved-caspase-3. Results. DNLA can significantly improve the viability and apoptosis rate of PC12 cell damage induced by Aβ25-35. It also can restore the reduced intracellular ROS content and MMP, while SOD activity and GSH content increase significantly. The expression of apoptosis-related protein Bax, cleaved-caspase-9, and cleaved-caspase-3 decreased when the Bcl-2 protein expression was significantly increased. Conclusion. These findings suggest that it can significantly inhibit the apoptosis of PC12 cell damage induced by Aβ25-35. The mechanism may reduce the level of cellular oxidative stress and thus inhibit the mitochondrial-mediated apoptosis pathway.

scholarly journals Protective Effects of Carvedilol and Vitamin C against Azithromycin-Induced Cardiotoxicity in Rats via Decreasing ROS, IL1-β, and TNF-αProduction and Inhibiting NF-κB and Caspase-3 Expression

2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
Nagla A. El-Shitany ◽  
Karema El-Desoky
Keyword(s):  
Lactate Dehydrogenase ◽  
Vitamin C ◽  
Glutathione Peroxidase ◽  
Caspase 3 ◽  
Apoptotic Cell ◽  
Interleukin 1 ◽  
Protective Effects ◽  
Histopathological Changes ◽  
Cardiovascular Risks ◽  
Necrosis Factor Alpha

The Food and Drug Administration recently warned of the fatal cardiovascular risks of azithromycin in humans. In addition, a recently published study documented azithromycin-induced cardiotoxicity in rats. This study aimed to justify the exact cardiovascular events accompanying azithromycin administration in rats, focusing on electrocardiographic, biochemical, and histopathological changes. In addition, the underlying mechanisms were studied regarding reactive oxygen species production, cytokine release, and apoptotic cell-death. Finally, the supposed protective effects of both carvedilol and vitamin C were assessed. Four groups of rats were used: (1) control, (2) azithromycin, (3) azithromycin + carvedilol, and (4) azithromycin + vitamin C. Azithromycin resulted in marked atrophy of cardiac muscle fibers and electrocardiographic segment alteration. It increased the heart rate, lactate dehydrogenase, creatine phosphokinase, malondialdehyde, nitric oxide, interleukin-1 beta (IL1-β), tumor necrosis factor alpha (TNF-α), nuclear factor kappa beta (NF-κB), and caspase-3. It decreased reduced glutathione, glutathione peroxidase, and superoxide dismutase. Carvedilol and vitamin C prevented most of the azithromycin-induced electrocardiographic and histopathological changes. Carvedilol and vitamin C decreased lactate dehydrogenase, malondialdehyde, IL1-β, TNF-α, NF-κB, and caspase-3. Both agents increased glutathione peroxidase. This study shows that both carvedilol and vitamin C protect against azithromycin-induced cardiotoxicity through antioxidant, immunomodulatory, and antiapoptotic mechanisms.

scholarly journals Antiepileptic Effects of Protein-Rich Extract from Bombyx batryticatus on Mice and Its Protective Effects against H2O2-Induced Oxidative Damage in PC12 Cells via Regulating PI3K/Akt Signaling Pathways

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Meibian Hu ◽  
Yujie Liu ◽  
Liying He ◽  
Xing Yuan ◽  
Wei Peng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Viability ◽  
Signaling Pathways ◽  
Pc12 Cells ◽  
Caspase 3 ◽  
Akt Signaling ◽  
Maximal Electroshock ◽  
Protective Effects ◽  
Caspase 9 ◽  
Protein Rich

Bombyx batryticatus is a known traditional Chinese medicine (TCM) utilized to treat convulsions, epilepsy, cough, asthma, headaches, and purpura in China for thousands of years. This study is aimed at investigating the antiepileptic effects of protein-rich extracts from Bombyx batryticatus (BBPs) on seizure in mice and exploring the protective effects of BBPs against H2O2-induced oxidative stress in PC12 cells and their underlying mechanisms. Maximal electroshock-induced seizure (MES) and pentylenetetrazole- (PTZ-) induced seizure in mice and the histological analysis were carried out to evaluate the antiepileptic effects of BBPs. The cell viability of PC12 cells stimulated by H2O2 was determined by MTT assay. The apoptosis and ROS levels of H2O2-stimulated PC12 cells were determined by flow cytometry analysis. Furthermore, the levels of malondialdehyde (MDA), superoxide dismutase (SOD), lactate dehydrogenase (LDH), and glutathione (GSH) in PC12 cells were assayed by ELISA and expressions of caspase-3, caspase-9, Bax, Bcl-2, PI3K, Akt, and p-Akt were evaluated by Western blotting and quantitative real-time polymerase chain reaction (RT-qPCR) assays. The results revealed that BBPs exerted significant antiepileptic effects on mice. In addition, BBPs increased the cell viability of H2O2-stimulated PC12 cells and reduced apoptotic cells and ROS levels in H2O2-stimulated PC12 cells. By BBPs treatments, the levels of MDA and LDH were reduced and the levels of SOD and GSH-Px were increased in H2O2-stimulated PC12 cells. Moreover, BBPs upregulated the expressions of PI3K, Akt, p-Akt, and Bcl-2, whereas they downregulated the expressions of caspase-9, caspase-3, and Bax in H2O2-stimulated PC12 cells. These findings suggested that BBPs possessed potential antiepileptic effects on MES and PTZ-induced seizure in mice and protective effects on H2O2-induced oxidative stress in PC12 cells by exerting antioxidative and antiapoptotic effects via PI3K/Akt signaling pathways.

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