Cellular Oxidative Damage Research Articles

Therapeutic and Health Promoting Potential of Terminalia chebula: An Exploratory Literature Review

: The plant Terminalia chebula has been used traditionally in many regions of the world for its therapeutic properties, especially in India. Its therapeutic and health-promoting potential has been recognized for centuries, and modern research continues to unveil its numerous benefits. One of the most significant applications of this plant is its antimicrobial and antioxidant potential. The plant contains high levels of phenolic compounds and flavonoids, which scavenge harmful free radicals in the body, reducing oxidative stress and cellular damage. This antioxidant action contributes to its anti-inflammatory effects, making it beneficial for a wide range of conditions, including arthritis, cardiovascular diseases, and neurodegenerative disorders. Furthermore, Terminalia chebula exhibits antimicrobial activity against various bacteria and fungi, including those responsible for common infections. It has been used to treat respiratory infections, urinary tract infections, and skin ailments. Its broad-spectrum antimicrobial effects make it a valuable natural remedy for combating microbial pathogens. Moreover, Terminalia chebula shows potential in managing diabetes and promoting cardiovascular health. Studies have indicated its ability to regulate blood sugar levels, improve insulin sensitivity, and reduce lipid abnormalities. These properties make it a promising adjunct therapy for individuals with diabetes or at risk of heart disease. In conclusion, Terminalia chebula possesses remarkable therapeutic and health-promoting potential. Its antioxidant, anti-inflammatory, antimicrobial, and digestive benefits make it a valuable natural remedy for various ailments. While research on Terminalia chebula is ongoing, its long-standing use in traditional medicine and emerging scientific evidence solidify its status as a potent medicinal plant with diverse applications in promoting overall well-being.

Extraction of Fucoxanthin from Marine Organisms and Its Therapeutic Effect on Cancer Cells

As China’s economy develops and its population grows, resources are becoming increasingly scarce. As a result, attention is shifting towards utilising marine resources, and the ability to process them is an increasingly important area of development.Within the traditional marine industry, kelp is primarily used for fucoidan extraction, with other substances such as kelp pigments often cast off as waste. Fucoxanthin constitutes the major carotenoid component found within kelp pigments. These pigments are believed to possess immunomodulatory, anti-inflammatory, and anti-tumour properties, and are of multifaceted benefit to human health by counteracting cellular oxidative damage induced by free radicals. Kelp served as the raw material in this study. Macroporous resin was utilized to extract Fucoxanthin from the kelp extract. Only an aqueous ethanol solution was employed for the extraction process. Subsequently, reduced-pressure column chromatography was conducted to quickly enrich the Fucoxanthin. Finally, the anti-tumour activity and free radical scavenging ability of the Fucoxanthin were analyzed. The results of the experiment revealed that Fucoxanthin can be effectively adsorbed by X-5 resin and its adsorption capability is robust. Additionally, using a 60% concentration of ethanol solution can promptly and effectively elute the absorbed Fucoxanthin from the X-5 resin. Moreover, after incubation for 48 hours at a concentration of 80 μg/mL of Fucoxanthin, the expression levels of p65, p52, and p50 genes significantly decreased in cancer cells. Fucoxanthin, a pigment found in kelp, exhibits potent antioxidant activity. The findings suggest that Fucoxanthin possesses the ability to effectively suppress the expression of cancer cells and scavenge free radicals.

Anti-diabetic effects of marine natural products through redox modulation via Nrf2/HO-1 cytoprotective pathways

Diabetes mellitus (DM), a major global health concern, is a chronic metabolic disorder. Bioactive compounds sourced from numerous marine natural products recently have drawn attention as novel therapeutic approaches. Considering these chemicals and their role in cellular redox modulation by involving the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) pathway, the current study attempts to highlight their anti-diabetic effects and the molecular mechanisms involved. Reactive oxygen species (ROS)-mediated oxidative stress, inflammation, and cellular damage are linked to most human pathologies specifically DM. The Nrf2/HO-1 pathway is a key defense mechanism developed by the cells to combat ROS burst. Marine natural compounds have strong pharmacological potential in triggering cellular antioxidant defense mechanisms by declining oxidative damage and inflammation linked to DM. How marine natural products potentially alleviate DM specifically type 2 diabetes (T2D) and its related issues is especially focused on. The literature was thoroughly analyzed to open a discussion about specific marine compounds and their well-established anti-diabetic effects to elucidate possible therapeutic applications. Furthermore, opportunities and the pros and cons of using these marine bioactive compounds as complementary treatment for DM are also discussed. The diverse characteristics of marine natural products, specifically with regard to redox control, offer promising opportunities for drug discovery and therapeutic interventions in clinical trials.

Therapeutic Potential of Melatonin: Multifaceted Applications in Muscle Health, Metabolic Disorders and Cardiovascular Disease

Melatonin, a hormone primarily synthesized by the pineal gland, is traditionally associated with the regulation of circadian rhythms. However, recent research has unveiled its broad spectrum of biological effects, positioning it as a valuable therapeutic agent in diverse health contexts. Known for its potent antioxidant and anti-inflammatory properties, melatonin plays a crucial role in maintaining homeostasis and protecting cellular integrity. This review explores melatonin’s therapeutic applications across multiple medical domains, including muscle health, metabolic disorders, chronic pain management, and cardiovascular health. In muscle health, melatonin facilitates muscle hypertrophy and regeneration by mitigating oxidative stress and enhancing the activity of satellite cells responsible for muscle repair. This action is particularly beneficial for individuals undergoing intense physical exertion, recovering from injuries, or combating age-related muscle. In metabolic disorders, such as type 2 diabetes, melatonin improves insulin sensitivity and reduces cellular oxidative damage, which supports beta-cell function and glucose regulation, potentially minimizing diabetes-related complications. Furthermore, in fibromyalgia - a condition marked by widespread pain and sleep disturbances - melatonin has demonstrated efficacy in alleviating pain and improving sleep quality, thus enhancing the overall quality of life for patients. In cardiovascular health, melatonin has shown promise in preventing and managing heart failure by reducing oxidative damage, modulating inflammatory pathways, and supporting endothelial function, which collectively contribute to improved cardiac health and reduced disease progression. This comprehensive review underscores melatonin’s emerging role as an integrative therapeutic agent in modern medicine.

Moisturizing and antioxidant factors of skin barrier restoring cream with shea butter, silkflo and vitamin E in human keratinocyte cells.

Moisturizers are integral to daily skincare routines, reflecting the increasing trend among people towards cosmetic products, particularly for skin care. They significantly contribute to preserving skin health, particularly by regulating the epidermal barrier and moisture levels within the skin. This study aims to explore the moisturizing and antioxidant effect of skin barrier restoring cream Moiz MM (MZ) with shea butter, silkflo and vitamin E by investigating its protective effect against oxidative stress-induced cellular damage and therapeutic mechanisms in human keratinocytes cells (HaCaT). The invitro antioxidant activity of MZ was evaluated by DPPH, ABTS and NO assays. For the cell culture study, HaCaT cells were cultured and stimulated using H2O2 and then treated with different concentrations of MZ. Then, it was subjected to DCFH-DA staining, reverse transcriptase PCR and western blot analysis for the evaluation of various skin-moisture-related components in human keratinocyte cells. Type I procollagen was examined using ELISA technique. The results highlighted that oxidative stress in HaCaT cells decreased type I procollagen synthesis, while MZ treatment significantly increased the synthesis. Moreover, the viability of HaCaT cells was not affected in the presence of MZ, which demonstrates its non-toxic effect. Furthermore, MZ can counteract H2O2-mediated oxidative stress by enhancing the antioxidant enzyme activity such as superoxide dismutase and catalase, and decrease reactive oxygen species generation in skin cells. Additionally, MZ greatly promotes hyaluronic acid production by enhancing the expression of the hyaluronic acid synthase-1 gene and Aquaporin 3 protein. This study suggests that MZ has the potential to serve as a moisturizing and antioxidant skincare formula.

Dual-Modality Accurate Visualization of Drug Synergy Based on Mass Spectrometry and Fluorescence Imaging.

There is a potential synergistic effect between nonsteroidal anti-inflammatory drugs and hydrogen sulfide (H2S), but direct evidence for the study is lacking. With a single fluorescence detection method, it is difficult to accurately confirm the effectiveness of the synergistic effect. In this study, the fluorescent probe and the nonsteroidal anti-inflammatory drug naproxen were combined via different self-immolative spacer groups to obtain a diagnostic and therapeutic integrated fluorescent probe Nap-NP-NSB, which can release H2S. The quantitative release of H2S by Nap-NP-NSB was evaluated in vitro and in cells, and the synergistic effect of H2S and naproxen was confirmed by monitoring the treatment process of cellular inflammation and oxidative damage of gastric mucosa cells. Finally, in vivo fluorescence imaging and mass spectrometry imaging of the liver and stomach tissues and their sections were performed in the mouse model of acute hepatitis. The dual-modal detection method not only confirmed that Nap-NP-NSB had better anti-inflammatory activity and less gastric mucosal damage, but also enabled a more accurate visualization of the drug synergistic effect of naproxen and H2S. This work provides a dual visualization imaging method combining fluorescence and mass spectrometry imaging and develops a new idea for studying drug synergies based on self-immolative structures.

Menstrual Blood-Derived Endometrial Stem Cells Ameliorate Ovarian Senescence by Relieving Oxidative Stress-Induced Inflammation.

Senescence is a degenerative process that occurs with ageing, and in the female reproductive system, senescence occurs earlier in the ovaries than in other tissues and organs, which implies a decrease in oocyte quality and exhaustion of the primordial follicular pool, leading to impaired ovarian function and an inability to maintain normal fertility. Unfortunately, the development of curative and effective treatments for ovarian senescence is still a considerable challenge. Currently, mesenchymal stem cells (MSCs)-based therapies for treating various refractory diseases, especially ovarian dysfunction, have been extensively studied and confirmed. However, the mechanisms by which MSCs improve ovarian senescence are not yet clear. Therefore, in this study, a mouse ageing model was generated via the intraperitoneal injection of a D-galactose (D-gal) solution, and the effects of menstrual blood-derived endometrial stem cells (MenSCs) transplantation on the ovarian follicle count, fibrosis level, and degree of apoptosis were evaluated. Subsequently, an ovarian granulosa cell ageing model was induced with H2O2, and CCK-8 assays, flow cytometry, mitochondrial membrane potential analysis and Western blotting were subsequently performed to further investigate the potential mechanism by which MenSCs ameliorate cellular oxidative damage. Overall, our findings demonstrated that MenSCs treatment can increase the cellular antioxidant capacity by activating the NRF2/HO-1 signalling pathway and further ameliorate the inflammatory ovarian microenvironment, apoptosis and dysfunction in ageing mice. These results provide reliable evidence and support for MenSCs-based therapy for ovarian senescence.

Molecular and Cellular Effects of Microplastics and Nanoplastics: Focus on Inflammation and Senescence.

Microplastics and nanoplastics (MNPs) are ubiquitous environmental contaminants. Their prevalence, persistence, and increasing industrial production have led to questions about their long-term impact on human and animal health. This narrative review describes the effects of MNPs on oxidative stress, inflammation, and aging. Exposure to MNPs leads to increased production of reactive oxygen species (ROS) across multiple experimental models, including cell lines, organoids, and animal systems. ROS can cause damage to cellular macromolecules such as DNA, proteins, and lipids. Direct interaction between MNPs and immune cells or an indirect result of oxidative stress-mediated cellular damage may lead to increased production of pro-inflammatory cytokines throughout different MNP-exposure conditions. This inflammatory response is a common feature in the pathogenesis of neurodegenerative, cardiovascular, and other age-related diseases. MNPs also act as cell senescence inducers by promoting mitochondrial dysfunction, impairing autophagy, and activating DNA damage responses, exacerbating cellular aging altogether. Increased senescence of reproductive cells and transfer of MNPs/induced damages from parents to offspring in animals further corroborates the transgenerational health risks of the tiny particles. This review aims to provoke a deeper investigation into the notorious effects these pervasive particles may have on human well-being and longevity.

Mitigation of Cisplatin-Induced Nephrotoxicity and Augmentation of Anticancer Potency via Tea Polyphenol Nanoparticles' Codelivery of siRNA from CRISPR/Cas9 Screened Targets.

Cisplatin, a frontline chemotherapeutic agent against cancer, faces challenges in clinical application due to significant toxicities and suboptimal efficacy. Renal toxicity, a dose-limiting factor of cisplatin, results from multifactorial processes including cisplatin-induced cellular pyroptosis, oxidative damage, and inflammatory responses. Our findings reveal that Tea Polyphenols Nanoparticles (TPNs) derived from Epigallocatechin gallate (EGCG) effectively could address these diverse mechanisms, comprehensively alleviating cisplatin-induced nephrotoxicity. Leveraging TPNs as carriers, chemical conjugation enables the encapsulation of tetravalent cisplatin prodrug, extending its systemic half-life, enhancing tumor tissue accumulation, while simultaneously mitigating renal toxicity. Concurrently, employing a CRISPR/Cas9 kinase library, we identified CSNK2A1 as a target sensitizing tumor cells to cisplatin, enabling specific siRNA sequences to augment cisplatin susceptibility, thereby minimizing the dosage requirement. Benefiting from the versatile carrier properties of TPNs to codeliver cisplatin prodrug and anti-CSNK2A1 siRNA, we developed a codelivery system, Pt-TPNs/siRNA. Pt-TPNs/siRNA not only enhances the anticancer effects but also mitigates cisplatin-induced renal toxicity, achieving efficacy while reducing toxicity. Mechanistic and safety assessments of these nanoparticles were conducted at both cellular and animal levels, opening new avenues for improved clinical utilization of cisplatin.

The Synergistic Effect of Intradialytic Concurrent Training and Melatonin Supplementation on Oxidative Stress and Inflammation in Hemodialysis Patients: A Double-Blind Randomized Controlled Trial

Background: This study aimed to investigate the effects of intradialytic concurrent (resistance–endurance) training combined with melatonin (MEL) supplementation on oxidative stress, inflammation, and cellular damage in hemodialysis (HD) patients. Methods: Thirty-two HD patients were randomly assigned to three groups: Exercise (EX)-MEL, EX-Placebo (PLA), and Control (C)-PLA. Participants in the EX-MEL and EX-PLA groups underwent 12 weeks of concurrent training. Before nocturnal sleep, they ingested either 3 mg of MEL (EX-MEL) or a placebo (EX-PLA and C-PLA). Blood samples were collected at baseline and after 12 weeks of intervention to assess lipid peroxidation [malondialdehyde (MDA)], antioxidant biomarkers [ferric-reducing antioxidant power (FRAP), reduced glutathione (GSH), total thiol (THIOL)], total bilirubin (TBIL), uric acid (UA), biomarkers of muscle and liver damage [aspartate aminotransferase (ASAT), alanine aminotransferase (ALAT), creatine kinase (CK), lactate dehydrogenase (LDH), and Gamma-glutamyltransferase (Gamma-GT)], and inflammation [C-reactive protein (CRP)]. Results: EX-MEL demonstrated a decrease in MDA (p < 0.05) and CRP (p < 0.05), and an increase in FRAP (p < 0.05) pre- and post-training. Both EX-MEL and EX-PLA showed an increase in GSH (p < 0.001, and p < 0.05, respectively) and THIOL (p < 0.01, and p < 0.05, respectively) pre- and post-training. No significant changes were observed in TBIL, UA, ASAT, ALAT, CK, LDH, or Gamma-GT pre- and post-training across all groups. Conclusion: Concurrent training combined with MEL supplementation enhances oxidant–antioxidant balance and reduces inflammation in HD patients more effectively than intradialytic concurrent training alone.

The impact of environmental microplastics as emerging carcinogens: A public health concern

Microplastics, small plastic particles less than 5 millimeters in size, have become common in the environment and occur in air, water, and food sources. Possible effects on human health, particularly as carcinogens, have become a growing concern. This review aims to investigate the mechanisms by which microplastics may contribute to cancer development and the implications for public health. A comprehensive literature review was conducted, focusing on studies from 2010 to 2024. The data were collected from various sources, including Google Scholar, PubMed, Web of Science and Scopus. The key areas examined include biological mechanisms of carcinogenesis, human exposure pathways, and risk assessment models. Microplastics can induce carcinogenesis through multiple pathways, including oxidative stress, inflammation, and cellular damage pathways. Research both in vivo and in vitro has demonstrated that microplastics can cause DNA damage and disrupt cellular processes, potentially leading to cancer. Human exposure occurs primarily through ingestion, inhalation, and dermal contact in the absence of data, and epidemiological studies indicate a link between increased levels of microplastic exposure and a greater risk of cancer. Microplastics represent a coming class of environmental carcinogens with significant public health implications. More investigations are needed to completely explain their carcinogenic mechanisms and to develop effective strategies to reduce human exposure. Public health policies must evolve to mitigate the risks connected with microplastic pollution, protecting future generations from its potential health impacts.

Proteomics Analysis on the Effects of Oxidative Stress and Antioxidants on Proteins Involved in Sterol Transport and Metabolism in Human Telomerase Transcriptase-Overexpressing-Retinal Pigment Epithelium Cells.

Age-related macular degeneration (AMD) is the most prevalent ocular disease in the elderly, resulting in blindness. Oxidative stress plays a role in retinal pigment epithelium (RPE) pathology observed in AMD. Tocopherols are potent antioxidants that prevent cellular oxidative damage and have been shown to upregulate the expression of cellular antioxidant proteins. Here, we determined whether oxidative stress and tocopherols, using either normal cellular conditions or conditions of sublethal cellular oxidative stress, alter the expression of proteins mediating sterol uptake, transport, and metabolism. Human telomerase transcriptase-overexpressing RPE cells (hTERT-RPE) were used to identify differential expression of proteins resulting from treatments. We utilized a proteomics strategy to identify protein expression changes in treated cells. After the identification and organization of data, we divided the identified proteins into groups related to biological function: cellular sterol uptake, sterol transport and sterol metabolism. Exposure of cells to conditions of oxidative stress and exposure to tocopherols led to similar protein expression changes within these three groups, suggesting that α-tocopherol (αT) and γ-tocopherol (γT) can regulate the expression of sterol uptake, transport and metabolic proteins in RPE cells. These data suggest that proteins involved in sterol transport and metabolism may be important for RPE adaptation to oxidative stress, and these proteins represent potential therapeutic targets.

Lipoic acid-functionalized platycodin D nanocarrier improves mitochondrial dysfunction and reverses diabetes

The prevalence of metabolic syndrome, particularly type 2 diabetes mellitus (T2DM), is steadily increasing on a global scale. It is widely acknowledged that multi-organ insulin resistance serves as the central pathological mechanism underlying T2DM. Mitochondrial dysfunction is recognized as a significant contributor to insulin resistance, with a focus on maintaining homeostasis and addressing cellular functional impairments. In recent years, the emergence of natural compounds has shed light on the potential of platycodin D (PD) in the realm of diabetes management. However, optimizing its bioavailability and targeted delivery within the intricate gastrointestinal system remains a critical challenge. This study involved the development of PD nanocarriers (PD NPs) through an enzymatic reaction, followed by lipoic acid esterification onto PD NPs to create mitochondrial-functionalized nanocarriers (PA NPs). Cell experiments demonstrated that PA NPs effectively targeted mitochondria and mitigated cellular oxidative damage. In vitro simulations revealed that PA NPs successfully navigated the gastric environment and reached the intestinal tract for controlled release. Animal studies showcased that PA NPs improved islet morphology and function, and its mechanism may be achieved by regulating the GSK3-β/IRS1/AMPK signal pathway cascade. Furthermore, PA NPs modulated the gut microbiota derangement in STZ-induced diabetic mice, driving a healthier state, species evenness, and abundance.

Performance Study and Application of Antioxidant Peptides CHCIWM and CHCPWM

AbstractWhen the level of reactive oxygen species (ROS) increases abnormally in the body, it damages tissue cells and is closely related to the occurrence of various chronic diseases. Antioxidant peptides (APs) are a class of active short peptides with antioxidant capacity, which have great research value. In this paper, two APs were designed and synthesized based on the structural features of APs: CHIWM (AP1) and CHCPWM (AP2). The reactive sites and activities of APs were analyzed using the quantum chemical density functional theory (DFT) method. The reactive sites are all located in the indolyl heterocycle of tryptophan residues, among which AP1 has a smaller energy gap and single point energy. Multiple free radical scavenging assays showed that AP1 and AP2 had stronger antioxidant activity than the positive control, glutathione (GSH). For scavenging DPPH free radicals, the IC50s values were 0.613 mg/mL and 0.606 mg/mL, respectively. In cellular assays, both AP1 and AP2 were able to scavenge ROS in the cells and attenuate cellular damage. In conclusion, AP1 and AP2 designed in this paper have good antioxidant activity and have the potential to be applied in the treatment of chronic diseases caused by cellular oxidative damage.

Glutathione Therapy in Diseases: Challenges and Potential Solutions for Therapeutic Advancement.

An endogenous antioxidant, reduced glutathione (GSH), is found at high concentrations in nearly all typical cells. GSH synthesis is a controlled process, and any disruption in the process of GSH synthesis could result in GSH depletion. Cellular oxidative damage results from GSH depletion. Various pathological conditions such as aging, cardiovascular disease (CVD), psychiatric disorders, neurological disorders, liver disorders, and diabetes mellitus are more affected by this stress. There are various reasons for GSH reduction, but replenishing it can help to improve this condition. However, there are challenges in this field. Low bioavailability and poor stability of GSH limit its delivery to tissues, mainly brain tissue. Today, new approaches are used for the optimal amount and efficiency of drugs and alternative substances such as GSH. The use of nano-materials and liposomes are effective methods for improving the treatment effects of GSH. The difficulties of GSH decrease and its connection to the most important associated disorders are reviewed for the first time in this essay. The other major concerns are the molecular mechanisms involved in them; the impact of treatment with replacement GSH; the signaling pathways impacted; and the issues with alternative therapies. The utilization of nano-materials and liposomes as potential new approaches to solving these issues is being considered.

Potentiated Calcium Carbonate with Enhanced Calcium Overload Induction and Acid Neutralization Capabilities to Boost Chemoimmunotherapy against Liver Cancer.

Unfavorable phenotypes characterized by low immunogenicity and acidity within the tumor microenvironment (TME) contribute to immunosuppression and therapeutic resistance. Herein, we rationally synthesized a multifunctional nanoregulator by encapsulating DOX and erianin into calcium carbonate (CaCO3)-based nanoparticles using a modified double emulsion method. The DOX and erianin-loaded CaCO3-based nanoparticles, termed DECaNPs, could effectively induce the calcium overload by triggering calcium influx and absorbing CaCO3 nanoparticles. Additionally, DECaNPs also neutralize the acidic TME by interacting with extracellular protons and limiting lactic acid production, a result of metabolic remodeling in cancer cells. As a result, DECaNPs elicit cellular oxidative stress damage, which mediates the activation of ferroptosis/apoptosis hybrid pathways, and profound immunogenic cell death. Treatment with DECaNPs could inhibit the growth of tumors by promoting oxidative stress, acid neutralization, metabolic remodeling, and protective antitumor immunity in vivo. In addition, DECaNPs could synergistically amplify the antitumor effects of αPD-L1 in a bilateral tumor model by eliciting systemic immune responses. In all, our work presents the preparation of CaCO3-based nanoregulators designed to reverse the unfavorable TME and enhance αPD-L1 immunotherapy through multiple mechanisms.

Study on the mechanism of ROS-induced oxidative stress injury and the broad-spectrum antimicrobial performance of nickel ion-doped V6O13 powder

In this study, pure V6O13 and nickel ion-doped V6O13 powders were synthesized by a simple hydrothermal-calcination method, and their broad-spectrum antimicrobial properties and mechanisms were investigated. The crystal structure, morphology, and chemical state of the powders were thoroughly analyzed by XRD, SEM, TEM, XPS, and UV–Vis. Their antimicrobial properties and mechanisms were evaluated by the ring of inhibition, bio-SEM, live-dead cell staining, ROS detection, and protein leakage experiments. The results showed that nickel ion doping modulated the oxygen defects of V6O13, generating more reactive oxygen species and leading to more severe oxidative stress, resulting in a broad-spectrum and highly efficient antimicrobial effect. This study also revealed the antimicrobial mechanism based on oxygen defect -induced ROS production, which caused cellular oxidative stress damage, leading to leakage of intracellular substances and cell death. This study not only demonstrates the potential of V6O13 as an efficient antimicrobial agent but also provides a strong experimental basis and theoretical support for the engineering design and optimization of novel antimicrobial materials by modulating material defects through ion doping.

Prospects of phycoerythrin: Structural features, antioxidation and applications in food

Phycoerythrin (PE) is a naturally occurring plant protein of algal origin. The colour, bioactivity and stability of PE are inextricably linked to its structure. PE has powerful antioxidant properties that effectively prevent oxidative stress and cellular damage, for which the chromophore structure plays a key role. However, the relationship between the chromophore and thermal stability is unclear in PE. The environmental factors affecting the thermal stability of PE are mainly light, high temperature and extreme pH. PE stability can be enhanced through various techniques, including the incorporation of additives, cross-linking processes, and the formation of complexes. Improving the stability of PE is of significant importance for its applications within the food industry. This paper outlines the structural characteristics of PE, discusses the relationship between its structure and antioxidant activity, and focuses on the application of PE in the food industry, as well as the factors affecting its stability and strategies for its improvement.

An innovative rheology analysis method applies to the formulation optimization of Panax notoginseng total saponins ocular gel

Emphasizing the viscoelasticity of ophthalmic gels is crucial for understanding the residence time, structure, and stability of hydrogels. This study primarily aimed to propose an innovative rheology analysis method for ophthalmic gels, considering complex eye movements. This method was applied to select ophthalmic gels with favorable rheological characteristics. Additionally, the physical characteristics and in vitro release of the selected Panax notoginseng total saponins (PNS) gel were demonstrated. The selected PNS gel significantly increased the activities of SOD and decreased intracellular levels of MDA, TNF-α, and IL-1β in H2O2-treated ARPE-19 cells. Finally, the optimal formulation was selected as a suitable platform for ophthalmic delivery and was shown to significantly rescue ARPE-19 cells from oxidative cellular damage.

Purine nucleoside phosphorylase as a target for the treatment of interstitial cystitis/bladder pain syndrome with and without Hunner lesions

Chronic visceral pain disorders, such as interstitial cystitis/bladder pain syndrome (IC/BPS), are difficult to treat, and therapies are limited in number and efficacy. Emerging evidence suggests that alterations in the enzyme purine nucleoside phosphorylase (PNPase) may participate in oxidative injury and cellular damage. PNPase is important for the metabolism of ‘tissue-protective’ purine metabolites to ‘tissue-damaging’ purines that generate free radicals. The aim of this study is to test whether patients living with IC/BPS without or with Hunner lesions and irrespective of any therapies exhibit purine dysregulation with higher levels of tissue-damaging purine metabolites as measured by liquid chromatography-tandem mass spectrometry. Our results demonstrate that levels of urotoxic purine metabolites (hypoxanthine and xanthine) in IC/BPS patients with and without Hunner lesions are elevated compared to healthy controls. These findings suggest there may be pathophysiologic commonalities between patient subtypes. Furthermore, the accumulation of uroprotective purines and depletion of urodamaging purines by PNPase inhibition may be therapeutically effective in both groups of patients.