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Acacia catechu Willd. Extract Protects Neuronal Cells from Oxidative Stress-Induced Damage.

ABSTRACT: Oxidative stress (OS) and the resulting reactive oxygen species (ROS) generation and inflammation play a pivotal role in the neuronal loss occurring during the onset of neurodegenerative diseases. Therefore, promising future drugs that would prevent or slow down the progression of neurodegeneration should possess potent radical-scavenging activity. Acacia catechu Willd. heartwood extract (AC), already characterized for its high catechin content, is endowed with antioxidant properties. The aim of the present study was to assess AC neuroprotection in both human neuroblastoma SH-SY5Y cells and rat brain slices treated with hydrogen peroxide. In SH-SY5Y cells, AC prevented a decrease in viability, as well as an increase in sub-diploid-, DAPI positive cells, reduced ROS formation, and recovered the mitochondrial potential and caspase-3 activation. AC related neuroprotective effects also occurred in rat brain slices as a reversal prevention in the expression of the main proteins involved in apoptosis and signalling pathways related to calcium homeostasis following OS-mediated injury. Additionally, unbiased quantitative mass spectrometry allowed for assessing that AC partially prevented the hydrogen peroxide-induced altered proteome, including proteins belonging to the synaptic vesicle fusion apparatus. In conclusion, the present results suggest the possibility of AC as a nutraceutical useful in preventing neurodegenerative diseases.

SUBMITTER: Chiaino E

PROVIDER: S-EPMC8773357 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Acacia Catechu Willd extract protects neuronal cells from oxidative stress-induced damage

Project description:Oxidative stress (OS) resulting in reactive oxygen species (ROS) generation and inflammation, play a pivotal role in the neuronal loss occurring in neurodegenerative diseases. Therefore, promising future drugs that would prevent or slow down the progression of neurodegeneration should possess potent radical-scavenging activity. Acacia catechu Willd heartwood extract (AC) contains high amount of catechins endowed of antioxidant properties. The aim of the present study was to assess AC neuroprotection in rat brain slices treated with hydrogen peroxide. AC reverted the decrease in viability as well as the increase in sub-diploid-, DAPI positive cells, reduced ROS formation, recovered the mitochondrial potential and caspase-3 activation. Neuroprotective effects occurred in rat brain slices as a reversal in the expression of the main proteins involved in apoptosis and signalling pathways related to calcium homeostasis following OS-mediated injury was demonstrated. Additionally, unbiased quantitative mass spectrometry allowed us to assess that AC partially reverted the hydrogen peroxide-induced altered proteome, including proteins belonging to the synaptic vesicle fusion apparatus. In conclusion, the present results suggest the possibility of AC as a nutraceutical useful in preventing neurodegenerative diseases.

2022-02-16 | PXD029239 | Pride

Apoptotic-Induced Effects of Acacia Catechu Willd. Extract in Human Colon Cancer Cells.

Project description:The research for innovative treatments against colon adenocarcinomas is still a great challenge. Acacia catechu Willd. heartwood extract (AC) has health-promoting qualities, especially at the gastrointestinal level. This study characterized AC for its catechins content and investigated the apoptosis-enhancing effect in human colorectal adenocarcinoma HT-29 cells, along with its ability to spare healthy tissue. MTT assay was used to describe the time course, concentration dependence and reversibility of AC-mediated cytotoxicity. Cell cycle analysis and AV-PI and DAPI-staining were performed to evaluate apoptosis, together with ROS formation, mitochondrial membrane potential (MMP) changes and caspase activities. Rat ileum and colon rings were tested for their viability and functionality to explore AC effects on healthy tissue. Quantitative analysis highlighted that AC was rich in (±)-catechin (31.5 ± 0.82 mg/g) and (-)-epicatechin (12.5 ± 0.42 mg/g). AC irreversibly decreased cell viability in a concentration-dependent, but not time-dependent fashion. Cytotoxicity was accompanied by increases in apoptotic cells and ROS, a reduction in MMP and increases in caspase-9 and 3 activities. AC did not affect rat ileum and colon rings' viability and functionality, suggesting a safe profile toward healthy tissue. The present findings outline the potential of AC for colon cancer treatment.

| S-EPMC7139529 | biostudies-literature

LC-HRMS Profiling and Antidiabetic, Antioxidant, and Antibacterial Activities of <i>Acacia catechu</i> (L.f.) Willd.

Project description:Acacia catechu (L.f.) Willd is a profoundly used traditional medicinal plant in Asia. Previous studies conducted in this plant are more confined to extract level. Even though bioassay-based studies indicated the true therapeutic potential of this plant, compound annotation was not performed extensively. This research is aimed at assessing the bioactivity of different solvent extracts of the plant followed by annotation of its phytoconstituents. Liquid chromatography equipped with high resolution mass spectrometry (LC-HRMS) is deployed for the identification of secondary metabolites in various crude extracts. On activity level, its ethanolic extract showed the highest inhibition towards α-amylase and α-glucosidase with an IC50 of 67.8 ± 1 μg/mL and 10.3 ± 0.1 μg/mL respectively, inspected through the substrate-based method. On the other hand, the plant extract showed an antioxidant activity of 23.76 ± 1.57 μg/mL, measured through radical scavenging activity. Similarly, ethyl acetate and aqueous extracts of A. catechu showed significant inhibition against Staphylococcus aureus with a zone of inhibition (ZoI) of 13 and 14 mm, respectively. With the LC-HRMS-based dereplication strategy, we have identified 28 secondary metabolites belonging to flavonoid and phenolic categories. Identification of these metabolites from A. catechu and its biological implication also support the community-based usage of this plant and its medicinal value.

| S-EPMC8380500 | biostudies-literature

Natural and induced polyploidy in Acacia dealbata Link. and Acacia mangium Willd.

Project description:Seeds were obtained from seven natural populations of Acacia dealbata, three natural populations of A. mangium and a seed orchard of A. mangium, representing the natural range of the two species. Polyploids were discovered in two of the seven populations of A. dealbata. The 2C DNA amount for diploid A. dealbata (2n = 2x = 26) was 1.74 pg, and for diploid A. mangium (2n = 2x = 26) was 1.30 pg. A naturally occurring tetraploid of A. dealbata (2n = 4x = 52) had a 2C DNA amount of 3.41 pg and a naturally occurring triploid genotype had a 2C DNA amount of 2.53 pg. The use of colchicine and oryzalin was investigated as a means of producing higher frequencies of tetraploids of both A. mangium and A. dealbata for incorporation into breeding programmes. Colchicine treatment gave tetraploid frequencies up to 29% for A. dealbata seedlings, and up to 18% for A. mangium seedlings. In contrast, no tetraploid A. mangium was detected following oryzalin treatment, and the low frequencies of tetraploids observed in A. dealbata could be attributed to their natural occurrence.

| S-EPMC4240402 | biostudies-literature

Aloin Protects Skin Fibroblasts from Heat Stress-Induced Oxidative Stress Damage by Regulating the Oxidative Defense System.

Project description:Oxidative stress is commonly involved in the pathogenesis of skin damage induced by environmental factors, such as heat stress. Skin fibroblasts are responsible for the connective tissue regeneration and the skin recovery from injury. Aloin, a bioactive compound in Aloe vera, has been reported to have various pharmacological activities, such as anti-inflammatory effects. The aim of this study was to investigate the protective effect of aloin against heat stress-mediated oxidative stress in human skin fibroblast Hs68 cells. Hs68 cells were first incubated at 43°C for 30 min to mimic heat stress. The study was further examined if aloin has any effect on heat stress-induced oxidative stress. We found that aloin protected Hs68 cells against heat stress-induced damage, as assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and lactate dehydrogenase assay. Aloin protected Hs68 cells by regulating reactive oxygen species production and increasing the levels of glutathione, cytosolic and mitochondrial superoxide dismutase. Aloin also prevented the elevation of thiobarbituric acid reactive substances and the reduction of 8-OH-dG induced by heat stress. These results indicated that aloin protected human skin fibroblasts from heat stress-induced oxidative stress damage by regulating the oxidative defense system.

| S-EPMC4670167 | biostudies-literature

Amaranth leaf extract protects against hydrogen peroxide induced oxidative stress in Drosophila melanogaster.

Project description:ObjectiveAmaranths leaves are rich in ascorbic acid and polyphenol compounds which have antioxidant activity. The aim of this study was to evaluate their in vivo antioxidant activity. The effect of consumption of Amaranth leaf extract on in vivo antioxidant activity, catalase enzyme activity and H2O2 induced oxidative stress in Drosophila melanogaster flies was assessed.ResultsConsumption of Amaranth leaf extract was associated with increased survival on exposure to H2o2 in a dose dependent manner in Drosophila melanogaster flies. The study concludes that the ethanolic extract of Amaranth leaves offer protection against hydrogen peroxide-induced oxidative stress.

| S-EPMC8130338 | biostudies-literature

Autophagy induction by SIRT6 is involved in oxidative stress-induced neuronal damage.

Project description:SIRT6 is a NAD(+)-dependent histone deacetylase and has been implicated in the regulation of genomic stability, DNA repair, metabolic homeostasis and several diseases. The effect of SIRT6 in cerebral ischemia and oxygen/glucose deprivation (OGD) has been reported, however the role of SIRT6 in oxidative stress damage remains unclear. Here we used SH-SY5Y neuronal cells and found that overexpression of SIRT6 led to decreased cell viability and increased necrotic cell death and reactive oxygen species (ROS) production under oxidative stress. Mechanistic study revealed that SIRT6 induced autophagy via attenuation of AKT signaling and treatment with autophagy inhibitor 3-MA or knockdown of autophagy-related protein Atg5 rescued H2O2-induced neuronal injury. Conversely, SIRT6 inhibition suppressed autophagy and reduced oxidative stress-induced neuronal damage. These results suggest that SIRT6 might be a potential therapeutic target for neuroprotection.

| S-EPMC4818841 | biostudies-literature

Mefenamic Acid-Upregulated Nrf2/SQSTM1 Protects Hepatocytes against Oxidative Stress-Induced Cell Damage.

Project description:Mefenamic acid (MFA) is a commonly prescribed non-steroidal anti-inflammatory drug (NSAID) with anti-inflammatory and analgesic properties. MFA is known to have potent antioxidant properties and a neuroprotective effect against oxidative stress. However, its impact on the liver is unclear. This study aimed to elucidate the antioxidative effects of MFA and their underlying mechanisms. We observed that MFA treatment upregulated the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway. Treatment with various anthranilic acid derivative-class NSAIDs, including MFA, increased the expression of sequestosome 1 (SQSTM1) in HepG2 cells. MFA disrupted the interaction between Kelch-like ECH-associated protein 1 (Keap1) and Nrf2, activating the Nrf2 signaling pathway. SQTM1 knockdown experiments revealed that the effect of MFA on the Nrf2 pathway was masked in the absence of SQSTM1. To assess the cytoprotective effect of MFA, we employed tert-Butyl hydroperoxide (tBHP) as a ROS inducer. Notably, MFA exhibited a protective effect against tBHP-induced cytotoxicity in HepG2 cells. This cytoprotective effect was abolished when SQSTM1 was knocked down, suggesting the involvement of SQSTM1 in mediating the protective effect of MFA against tBHP-induced toxicity. In conclusion, this study demonstrated that MFA exhibits cytoprotective effects by upregulating SQSTM1 and activating the Nrf2 pathway. These findings improve our understanding of the pharmacological actions of MFA and highlight its potential as a therapeutic agent for oxidative stress-related conditions.

| S-EPMC10536671 | biostudies-literature

Acanthus ebracteatus leaf extract provides neuronal cell protection against oxidative stress injury induced by glutamate.

Project description:BackgroundAcanthus ebracteatus (AE), an herb native to Asia, has been recognized in traditional folk medicine not only for its antioxidant properties and various pharmacological activities but also as an ingredient of longevity formulas. However, its anti-neurodegenerative potential is not yet clearly known. This work aimed to evaluate the protective effect of AE leaf extract against glutamate-induced oxidative damage in mouse hippocampal HT22 cells, a neurodegenerative model system due to a reduction in glutathione levels and an increase in reactive oxygen species (ROS).MethodsCell viability, apoptosis, and ROS assays were performed to assess the protective effect of AE leaf extract against glutamate-induced oxidative toxicity in HT22 cells. The antioxidant capacity of AE was evaluated using in vitro radical scavenging assays. The subcellular localization of apoptosis-inducing factor (AIF) and the mRNA and protein levels of genes associated with the nuclear factor erythroid 2-related factor 2 (Nrf2) antioxidant system were determined to elucidate the mechanisms underlying the neuroprotective effect of AE leaf extract.ResultsWe demonstrated that AE leaf extract is capable of attenuating the intracellular ROS generation and HT22 cell death induced by glutamate in a concentration-dependent manner. Co-treatment of glutamate with the extract significantly reduced apoptotic cell death via inhibition of AIF nuclear translocation. The increases in Nrf2 levels in the nucleus and gene expression levels of antioxidant-related downstream genes under Nrf2 control were found to be significant in cells treated with the extract.ConclusionsThe results suggested that AE leaf extract possesses neuroprotective activity against glutamate-induced oxidative injury and may have therapeutic potential for the treatment of neurodegenerative diseases associated with oxidative stress.

| S-EPMC6192065 | biostudies-literature

Mitochondrial Ferritin Protects Hydrogen Peroxide-Induced Neuronal Cell Damage.

Project description:Oxidative stress and iron accumulation are tightly associated with neurodegenerative diseases. Mitochondrial ferritin (FtMt) is identified as an iron-storage protein located in the mitochondria, and its role in regulation of iron hemeostasis in neurodegenerative diseases has been reported. However, the role of FtMt in hydrogen peroxide (H2O2)-induced oxidative stress and iron accumulation in neuronal cells has not been studied. Here, we overexpressed FtMt in neuroblastoma SH-SY5Y cells and induced oxidative stress by treating with extracellular H2O2. We found that overexpression of FtMt significantly prevented cell death induced by H2O2, particularly the apoptosis-dependent cell death. The protective effects involved inhibiting the generation of cellular reactive oxygen species, sustaining mitochondrial membrane potential, maintaining the level of anti-apoptotic protein Bcl-2, and inhibiting the activation of pro-apoptotic protein caspase 3. We further explored the mechanism of these protective effects and found that FtMt expression markedly altered iron homeostasis of the H2O2 treated cells as compared to that of controls. The FtMt overexpression significantly reduced cellular labile iron pool (LIP) and protected H2O2-induced elevation on LIP. While in H2O2 treated SH-SY5Y cells, the increased iron uptake and reduced iron release, in correlation with levels of DMT1(-IRE) and ferroportin 1, resulted in heavy iron accumulation, the FtMt overexpressing cells didn't show any significant changes in levels of iron transport proteins and in the level of LIP. These results implicate a neuroprotective role of FtMt on H2O2-induced oxidative stress, which may provide insights into the treatment of iron accumulation associated neurodegenerative diseases.

| S-EPMC5524808 | biostudies-other

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