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Food & Function Nov 2023Lycopene is an important pigment with an alkene skeleton from , which is also obtained from some red fruits and vegetables. Lycopene is used in the food field with rich... (Review)
Review
Lycopene is an important pigment with an alkene skeleton from , which is also obtained from some red fruits and vegetables. Lycopene is used in the food field with rich functions and serves in the medical field with multiple clinical values because it has dual functions of both medicine and food. It was found that lycopene was mainly isolated by solvent extraction, ultrasonic-assisted extraction, supercritical fluid extraction, high-intensity pulsed electric field-assisted extraction, enzymatic-assisted extraction, and microwave-assisted extraction. Meanwhile, it was also obtained 2 synthetic pathways: chemical synthesis and biosynthesis. Pharmacological studies revealed that lycopene has anti-oxidant, hypolipidemic, anti-cancer, immunity-enhancing, hepatoprotective, hypoglycemic, cardiovascular-protective, anti-inflammatory, neuroprotective, and osteoporosis-inhibiting effects. The application of lycopene mainly includes food processing, animal breeding, and medical cosmetology fields. It is hoped that this review will provide some useful information and guidance for future study and exploitation of lycopene.
Topics: Lycopene; Carotenoids; Antioxidants; Fruit; Solanum lycopersicum
PubMed: 37916682
DOI: 10.1039/d3fo03327a -
International Journal of Molecular... Mar 2024The brain is susceptible to oxidative stress, which is associated with various neurological diseases. Edaravone (MCI-186, 3-methyl-1 pheny-2-pyrazolin-5-one), a free... (Review)
Review
The brain is susceptible to oxidative stress, which is associated with various neurological diseases. Edaravone (MCI-186, 3-methyl-1 pheny-2-pyrazolin-5-one), a free radical scavenger, has promising effects by quenching hydroxyl radicals (∙OH) and inhibiting both ∙OH-dependent and ∙OH-independent lipid peroxidation. Edaravone was initially developed in Japan as a neuroprotective agent for acute cerebral infarction and was later applied clinically to treat amyotrophic lateral sclerosis (ALS), a neurodegenerative disease. There is accumulating evidence for the therapeutic effects of edaravone in a wide range of diseases related to oxidative stress, including ischemic stroke, ALS, Alzheimer's disease, and placental ischemia. These neuroprotective effects have expanded the potential applications of edaravone. Data from experimental animal models support its safety for long-term use, implying broader applications in various neurodegenerative diseases. In this review, we explain the unique characteristics of edaravone, summarize recent findings for specific diseases, and discuss its prospects for future therapeutic applications.
Topics: Animals; Female; Pregnancy; Amyotrophic Lateral Sclerosis; Antioxidants; Antipyrine; Edaravone; Free Radical Scavengers; Neurodegenerative Diseases; Neuroprotective Agents; Placenta
PubMed: 38474192
DOI: 10.3390/ijms25052945 -
Toxicology and Industrial Health Oct 2023Most of the literature has focused on titanium dioxide (TiO) nanoparticles (NPs) toxicity, showing the importance of oxidative stress, mitochondrial dysfunction, and...
Most of the literature has focused on titanium dioxide (TiO) nanoparticles (NPs) toxicity, showing the importance of oxidative stress, mitochondrial dysfunction, and cell death in TiO-induced toxicity. For this purpose, in the current study, we investigated the protective role of antioxidant and mitochondrial/lysosomal protective agents to minimize TiO NPs-induced toxicity in human lymphocytes. Human lymphocytes were obtained from heathy individuals and treated with different concentrations (80, 160, and 320 µg/mL) of TiO NPs, and then human lymphocytes preincubated with butylated hydroxytoluene (BHT), cyclosporin A (CsA), and chloroquine separately were exposed to TiO NPs for 6 h. In all the above-mentioned treated groups, adverse parameters such as cytotoxicity, reactive oxygen species (ROS), mitochondrial membrane potential (MMP), lysosomal membrane destabilization, the levels of malondialdehyde (MDA), and glutathione (GSH) were measured. The results showed that TiO nanoparticles induced cytotoxicity through ROS formation, MMP collapse, lysosomal damages, depletion of GSH, and lipid peroxidation. However, BHT as an antioxidant, CsA as a mitochondrial permeability transition (MPT) pore sealing agent, and chloroquine as a lysosomotropic agent, significantly inhibited all the TiO NPs-induced cellular and organelle toxicities. Thus, it seems that antioxidant and mitochondrial/lysosomal protective agents are promising preventive strategies against TiO NPs-induced toxicity.
Topics: Humans; Antioxidants; Reactive Oxygen Species; Protective Agents; Lysosomes; Mitochondria; Glutathione; Chloroquine; Lymphocytes; Nanoparticles
PubMed: 37593903
DOI: 10.1177/07482337231196293 -
Current Molecular Pharmacology 2024Ischemia and reperfusion damage to the liver is one of the major causes of hepatic dysfunction and liver failure after a liver transplant. The start of hepatic...
Ischemia and reperfusion damage to the liver is one of the major causes of hepatic dysfunction and liver failure after a liver transplant. The start of hepatic ischemia-reperfusion damage is linked to metabolic acidosis, Kupffer cells, neutrophils, excessive calcium, and changes in the permeability of the mitochondrial membrane. Hypoxia activates Kupffer cells, resulting in the production of reactive oxygen species (ROS). These ROS when accumulated, causes apoptosis and necrosis, as well as activate immune and inflammatory responses that involve many cells and signalling molecules. Numerous antioxidant compounds have been researched to lessen oxidative stress and thus serve as potential compounds to deal the ischemia-reperfusion damage. This article confers a deep understanding of the protective effects of some effective therapies, including hepatoprotective agents, attenuation of an increase in xanthine oxidase activity, and administration of antioxidants like N-acetylcysteine, superoxide dismutase (SOD), and ornithine.
Topics: Humans; Reactive Oxygen Species; Liver; Reperfusion Injury; Acetylcysteine; Antioxidants; Ischemia
PubMed: 37534481
DOI: 10.2174/1874467217666230803114856 -
Experimental Neurology Apr 2024Stroke is one of the leading causes of death and long-term disability worldwide. Previous studies have found that corilagin has antioxidant, anti-inflammatory,...
Integrated network pharmacology, molecular docking and pharmacodynamic study reveals protective effects and mechanisms of corilagin against cerebral ischemia-induced injury.
BACKGROUND
Stroke is one of the leading causes of death and long-term disability worldwide. Previous studies have found that corilagin has antioxidant, anti-inflammatory, anti-atherosclerotic and other pharmacological activities and has a protective effect against cardiac and cerebrovascular injury.
OBJECTIVES
The aim of this study was to investigate the protective effects of corilagin against ischemic stroke and to elucidate the underlying molecular mechanisms using network pharmacology, molecular docking, and animal and cell experiments.
METHODS
We investigated the potential of corilagin to ameliorate cerebral ischemia-reperfusion injury using in vivo rat middle cerebral artery occlusion/reperfusion (MCAO/R) and in vitro oxygen-glucose deprivation/reoxygenation (OGD/R) models.
RESULTS
Our results suggest that corilagin may exert its anti-ischemic stroke effect by interacting with 92 key targets, including apoptosis-associated proteins (Bcl-2, Bax, caspase-3) and PI3K/Akt signaling pathway-related proteins. In vivo and in vitro experiments showed that corilagin treatment improved neurological deficits, attenuated cerebral infarct volume, and mitigated neuronal damage in MCAO/R rats. Corilagin treatment also enhanced the survival of PC12 cells exposed to OGD/R, reduced the rate of LDH leakage, inhibited cell apoptosis, and activated the PI3K/Akt signaling pathway. Importantly, the effects of corilagin on the PI3K/Akt signaling pathway and apoptosis-associated proteins were reversed by the PI3K-specific inhibitor LY294002.
CONCLUSIONS
These results indicate that the molecular mechanism of the anti-ischemic effect of corilagin involves inhibiting neuronal apoptosis and activating the PI3K/Akt signaling pathway. These findings provide a theoretical and experimental basis for the further development and application of corilagin as a potential anti-ischemic stroke agent.
Topics: Rats; Animals; Molecular Docking Simulation; Proto-Oncogene Proteins c-akt; Phosphatidylinositol 3-Kinases; Network Pharmacology; Rats, Sprague-Dawley; Brain Ischemia; Infarction, Middle Cerebral Artery; Reperfusion Injury; Neuroprotective Agents; Brain Injuries; Apoptosis; Glucosides; Hydrolyzable Tannins
PubMed: 38266765
DOI: 10.1016/j.expneurol.2024.114697 -
Biotechnology Journal Feb 2024Organoid technology has demonstrated unique advantages in multidisciplinary fields such as disease research, tumor drug sensitivity, clinical immunity, drug toxicology,... (Review)
Review
Organoid technology has demonstrated unique advantages in multidisciplinary fields such as disease research, tumor drug sensitivity, clinical immunity, drug toxicology, and regenerative medicine. It will become the most promising research tool in translational research. However, the long preparation time of organoids and the lack of high-quality cryopreservation methods limit the further application of organoids. Although the high-quality cryopreservation of small-volume biological samples such as cells and embryos has been successfully achieved, the existing cryopreservation methods for organoids still face many bottlenecks. In recent years, with the development of materials science, cryobiology, and interdisciplinary research, many new materials and methods have been applied to cryopreservation. Several new cryopreservation methods have emerged, such as cryoprotectants (CPAs) of natural origin, ice-controlled biomaterials, and rapid rewarming methods. The introduction of these technologies has expanded the research scope of cryopreservation of organoids, provided new approaches and methods for cryopreservation of organoids, and is expected to break through the current technical bottleneck of cryopreservation of organoids. This paper reviews the progress of cryopreservation of organoids in recent years from three aspects: damage factors of cryopreservation of organoids, new protective agents and loading methods, and new technologies of cryopreservation and rewarming.
Topics: Cryopreservation; Cryoprotective Agents; Organoids; Regenerative Medicine
PubMed: 38403430
DOI: 10.1002/biot.202300543 -
Toxicology Aug 2023Ischemic stroke is regarded one of the most common causes of brain vulnerability. Silibinin (SIL), extracted from the seeds of Silybinisus laborinum L., has been found...
Ischemic stroke is regarded one of the most common causes of brain vulnerability. Silibinin (SIL), extracted from the seeds of Silybinisus laborinum L., has been found to exhibit obvious therapeutic effects on neurodegenerative diseases. GAS6 has been proven to have significant neuroprotective effects; however, the role of SIL and GAS6 in ischemic stroke remains unclear. This study aimed to investigate the protective effects of SIL against cerebral ischemia-reperfusion injury in neuroblastoma N2a cells, as well as the mechanisms involved. Firstly, the toxicity of SIL was evaluated, and safe concentrations were chosen for subsequent experiments. Then, SIL exerts significant neuroprotection against hypoxia/reoxygenation (HR) injury in N2a cells, as manifested by increased cell viability, decreased apoptotic rate, LDH, and ROS generation. Additionally, SIL was found to inhibit HR-induced apoptosis, mitochondria dysfunction, and oxidative stress. However, silencing of GAS6 inhibited the neuroprotective effects of SIL. To sum up, these results suggest that SIL may be a promising therapeutic agent for the treatment of ischemic stroke.
Topics: Humans; Neuroprotective Agents; Silybin; Hypoxia; Hypoxia, Brain; Ischemic Stroke; Apoptosis
PubMed: 37544575
DOI: 10.1016/j.tox.2023.153598 -
European Review For Medical and... Nov 2023The present research aimed to study the possible protective effects of Silymarin on testicular I/R injury in a rat model evaluated through histopathology and biochemical...
OBJECTIVE
The present research aimed to study the possible protective effects of Silymarin on testicular I/R injury in a rat model evaluated through histopathology and biochemical parameters.
MATERIALS AND METHODS
This research investigated the impact of Silymarin on IR damage in male Wistar albino rats. Animals were divided into three groups: group 1 (sham), group 2 (IR), and group 3 (IR+Silymarin).
RESULTS
There were no notable differences in the levels of malondialdehyde (MDA), myeloperoxidase (MPO), and glutathione (GSH) across the three groups (p=0.260, p=0.486 and p=0.803, respectively). Contrarily, the total antioxidant status (TAS) levels exhibited significant variations between groups (p=0.001). The total oxidant status (TOS) levels also differed significantly between groups (p=0.004). The tissue evaluations uncovered substantial differences in the Johnson score, which is used to gauge testicular damage. A distinct contrast was seen between Group 1 and Group 2, and also between Group 2 and Group 3, with an all-encompassing p-value lower than 0.01. The same significant disparities were found for the percentages of Bax and Annexin V immunostaining (p<0.01 for each), reflecting the inflammation and apoptosis brought about by ischemia-reperfusion and the protective effects of the treatment.
CONCLUSIONS
The outcomes of the current investigation showed that Silymarin could be a valuable agent for reducing testicular tissue damage following I/R injury.
Topics: Humans; Rats; Male; Animals; Spermatic Cord Torsion; Rats, Wistar; Silymarin; Oxidative Stress; Reperfusion Injury; Testis; Antioxidants; Glutathione; Malondialdehyde
PubMed: 37975368
DOI: 10.26355/eurrev_202311_34319 -
European Journal of Pharmacology Nov 2023Intracerebral hemorrhage (ICH) is the most devastating subtype of stroke, nevertheless specific treatments with conclusive clinical benefit in improving outcomes of ICH...
Intracerebral hemorrhage (ICH) is the most devastating subtype of stroke, nevertheless specific treatments with conclusive clinical benefit in improving outcomes of ICH remain lacking. The present study applied dl-3-n-butylphthalide (NBP), a compound approved for the treatment of ischemic stroke and rarely studied in ICH, to an experimental animal model of ICH, aiming to evaluate the therapeutic effects of NBP on ICH and the potential mechanisms. The results showed that rats receiving NBP administration exhibited a structural and functional restoration of brain after ICH mainly manifested as alleviation of neuronal apoptosis, suppression of neuroinflammation and oxidative stress, neurovascular remodeling, and eventually improvement of neurological deficits. In addition, several protein targets of NBP were revealed, which mainly play molecular functions of ribonucleoside triphosphate phosphatase activity, pyrophosphatase activity, hydrolase activity and GTPase activity, and participate in the biological process of brain development by regulating the formation of cellular components such as spindles, polymeric cytoskeletal fibers, microtubules and synapses, through mediating pathways such as VEGF signaling pathway, Fc epsilon RI signaling pathway, ECM-receptor interaction, Fc gamma R-mediated phagocytosis, peroxisome and so on, guiding the mechanism exploration of NBP therapy to some extent. Taken together, the study added some new evidence to the application of NBP in ICH treatment.
Topics: Rats; Animals; Neuroprotective Agents; Brain; Cerebral Hemorrhage; Stroke
PubMed: 37802280
DOI: 10.1016/j.ejphar.2023.176105 -
Neurochemistry International Nov 2023Intracerebral hemorrhage (ICH), which has high mortality and disability rate is associated with microglial pyroptosis and neuroinflammation, and the effective treatment...
Intracerebral hemorrhage (ICH), which has high mortality and disability rate is associated with microglial pyroptosis and neuroinflammation, and the effective treatment methods are limited Epigallocatechin-3-gallate (EGCG) has been found to play a cytoprotective role by regulating the anti-inflammatory response to pyroptosis in other systemic diseases. However, the role of EGCG in microglial pyroptosis and neuroinflammation after ICH remains unclear. In this study, we investigated the effects of EGCG pretreatment on neuroinflammation-mediated neuronal pyroptosis and the underlying neuroprotective mechanisms in experimental ICH. EGCG pretreatment was found to remarkably improved neurobehavioral performance, and decreased the hematoma volume and cerebral edema in mice. We found that EGCG pretreatment attenuated the release of hemin-induced inflammatory cytokines (IL-1β, IL-18, and TNF-α). EGCG significantly upregulated the expression of heme oxygenase-1 (HO-1), and downregulated the levels of pyroptotic molecules and inflammatory cytokines including Caspase-1, GSDMD, NLRP3, mature IL-1β, and IL-18. EGCG pretreatment also decreased the number of Caspase-1-positive microglia and GSDMD along with NLRP3-positive microglia after ICH. Conversely, an HO-1-specific inhibitor (ZnPP), significantly inhibited the anti-pyroptosis and anti-neuroinflammation effects of EGCG. Therefore, EGCG pretreatment alleviated microglial pyroptosis and neuroinflammation, at least in part through the Caspase-1/GSDMD/NLRP3 pathway by upregulating HO-1 expression after ICH. In addition, EGCG pretreatment promoted the polarization of microglia from the M1 phenotype to M2 phenotype after ICH. The results suggest that EGCG is a potential agent to attenuate neuroinflammation via its anti-pyroptosis effect after ICH.
Topics: Animals; Mice; Caspases; Cerebral Hemorrhage; Cytokines; Heme Oxygenase-1; Interleukin-18; Microglia; Neuroinflammatory Diseases; NLR Family, Pyrin Domain-Containing 3 Protein; Pyroptosis; Antioxidants; Neuroprotective Agents
PubMed: 37633650
DOI: 10.1016/j.neuint.2023.105603