Hesperidin Inhibits Oral Cancer Cell Growth via Apoptosis and Inflammatory Signaling-Mediated Mechanisms: Evidence From In Vitro and In Silico Analyses DOI Open Access

Selvaraj Jayaraman,

Sathanraj Natararaj,

Vishnu Priya Veeraraghavan

и другие.

Cureus, Год журнала: 2024, Номер unknown

Опубликована: Фев. 2, 2024

Background Oral carcinoma presents a significant health challenge, prompting the need for innovative therapeutic approaches. Elevation of inflammatory mediators, including tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), has promoted cellular proliferation, inhibited apoptosis, fostered oral cancer progression through complex signaling pathways. Hesperidin, flavanone glycoside found in citrus fruits, is keen interest this study as it been proven to have multiple benefits vivo vitro studies. However, mechanism behind anticancer activity hesperidin remains obscure. Aim The aimed explore potential on human cells (KB cells) by modulating pro-inflammatory apoptotic mechanisms. Methods Cancer cell growth inhibitory was assessed using MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide) assay. Gene expression analysis performed real-time RT-PCR analysis. In addition, silico docking conducted confirm binding affinity with apoptosis molecules. data were analyzed one-way ANOVA "t" test. Results Utilizing assay, dose-dependent cytotoxic effect unveiled, remarkable IC50 value indicative its potent inhibition proliferation. Complementing these findings (p<0.05), qRT-PCR demonstrated hesperidin's regulatory influence key molecular targets within KB line. Hesperidin treatment resulted noteworthy reduction TNF-α, interleukin-1 beta (IL-1-β), IL-6, nuclear factor kappa-light-chain-enhancer activated B (NF-κB), B-cell lymphoma 2 (Bcl-2) mRNA levels highlighting role migration, inflammation processes. Simultaneously, BAX indicating an enhancement death. Molecular simulations further revealed robust affinities between target proteins, suggesting disrupt functions pathways cells. Conclusion effects line anti-inflammatory properties position compelling candidate exploration quest effective treatments. These shed light intricate mechanisms underlying promise agent against carcinoma.

Язык: Английский

High energy diet-induced prediabetic neuropathic pain is mediated by reduction of SIRT6 negative control of both spinal and peripheral neuroinflammation DOI
Yan Yang, Wei Sun, Fan Yang

и другие.

Neuroscience, Год журнала: 2025, Номер unknown

Опубликована: Фев. 1, 2025

Язык: Английский

Процитировано

0

Febuxostat protects from Doxorubicin induced hepatotoxicity in rats via regulation of NF-κB p65/NLRP3 inflammasome and SIRT-1/AMPK pathways DOI Creative Commons
Ahmed M. El‐Dessouki,

Eman H. Yousef,

Nahed A. Raslan

и другие.

Naunyn-Schmiedeberg s Archives of Pharmacology, Год журнала: 2025, Номер unknown

Опубликована: Фев. 14, 2025

Abstract Doxorubicin (DOX) is a highly potent broad-spectrum anticancer drug, but it has severe side effects, including hepatotoxicity. Therefore, we evaluated the efficacy of febuxostat (FBX), specific inhibitor xanthine oxidase and antioxidant, in blocking hepatotoxicity associated with DOX rats. Rats were treated FBX (10 or 15 mg/kg/day orally for 2 weeks) given (15 mg/kg as single dose at 7th day, intraperitoneal) to induce The results indicated that could reduce pathological alterations liver tissues induced by ameliorate inappropriate changes function biomarkers (AST, ALT, ALP) serum, oxidative stress parameters (catalase, superoxide dismutase, NOX1, NQO-1, HO-1, Keap-1, Nrf2) inflammatory markers (NF-κB p65, TNF-α, NLRP3). Additionally, attenuated p53, BAX, cytochrome C, caspase-9, caspase-3 levels restrain cell apoptosis. In addition, therapy was found increase protein SIRT-1 AMPK liver. These findings demonstrate can caused rats through mechanisms counteract stress, inflammation,

Язык: Английский

Процитировано

0

Changes in MMP-9, T-SOD and SIRT-1 levels after non-surgical periodontal treatment DOI Creative Commons

Sezgi İyigün,

Nimet Gül Görgülü, Başak Doğan

и другие.

BMC Oral Health, Год журнала: 2025, Номер 25(1)

Опубликована: Фев. 19, 2025

Matrix metalloproteinase-9 (MMP-9), total superoxide dismutase (T-SOD) and sirtuin (SIRT)-1 are interrelated molecules linked with oxidative stress periodontitis pathogenesis which may have implications for both the diagnosis of or efficacy periodontal treatment. This study aimed to evaluate salivary serum MMP-9, T-SOD, SIRT-1 levels in stage 3 patients (P-S3) following non-surgical treatment (NSPT). Forty-nine subjects, comprising 17 healthy, 16 P-S3 Grade B (P-S3GB), C (P-S3GC) participated study. Clinical parameters, T-SOD were evaluated at baseline from all participants 3-months patients. Enzyme-linked immunosorbent assay (ELISA) was used assess biochemical parameters. All clinical parameters improved groups (p < 0.05) after NSPT. In P-S3GB GC groups, MMP-9 higher than healthy controls decreased NSPT 0.05). P-S3GC group had ones Salivary similar among > After NSPT, only group, decreased, increased showed positive correlations The results suggest that potential biomarkers diagnosing evaluating However, further research is necessary validate these findings across grades stages periodontitis. retrospectively registered on 13/02/2024 trials.gov number NCT06255470.

Язык: Английский

Процитировано

0

Protective effect of roflumilast on cyclophosphamide-induced ovarian toxicity in rats: role of SIRT1/Nrf2/nF-ĸB pathway DOI
Salma A. El-Marasy,

Hadir Farouk,

Marwa S. Khattab

и другие.

Immunopharmacology and Immunotoxicology, Год журнала: 2025, Номер unknown, С. 1 - 10

Опубликована: Март 25, 2025

This study aimed to investigate the possible protective effect of roflumilast (RFL) on cyclophosphamide (CP)-induced ovarian toxicity as well underlying mechanism. Female Wistar rats received vehicle (n = 6) or CP (200 mg/kg, i.p.). The other 2 groups 6 for each) were orally pretreated with RFL at dosages 0.5 and 1 respectively, 14 days then after one hour administration 14th day, intraperitoneally administered a single dose CP. Serum tissue samples collected. Biochemical, real-time polymerase chain reaction, histopathological immunohistopathological examination carried out. significantly elevated serum follicle-stimulating hormone (FSH) luteinizing (LH) compared group. remarkably contents Sirtuin-1 (SIRT1), heme oxygenase-1 (HO-1), reduced nuclear factor-kappa B (NF-ĸb) p65/NF-ĸB ratio control Compared group, Nrf2 gene expression, malondialdehyde (MDA), glutathione (GSH) content. It also protein expression TNF-α caspase-3. can be concluded that (0.5 mg/kg) protected against CP-induced via altering SIRT1/Nrf2/NF-ĸB pathway, ameliorating changes in addition its anti-apoptotic effect.

Язык: Английский

Процитировано

0

Increased Oxidative Stress and Decreased Sirtuin-3 and FOXO3 Expression Following Carotid Artery Intimal Injury in Hyperlipidemic Yucatan Microswine DOI

Prathosh Velpuri,

Parth Patel,

Armand N Yazdani

и другие.

Cardiology and Cardiovascular Medicine, Год журнала: 2024, Номер 08(01)

Опубликована: Янв. 1, 2024

Hypercholesterolemia is a major risk factor for atherosclerosis as oxidized-low-density lipoproteins (ox-LDL) contribute to the formation of foam cells and inflammation. Increased immune cell infiltration oxidative stress induce instability plaque. Rupture unstable plaque precipitates adverse ischemic events. Since reactive oxygen species (ROS) play critical role in vulnerability, regulating ROS generation may have therapeutic potential. Sirtuins, specifically sirtuin-3 (SIRT3), are antigenic molecules that can reduce by reducing mitochondrial production through epigenetic modulation. Lack SIRT3 expression associated with dysregulation endothelial function following high-fat high-cholesterol diet. deacetylates FOXO3a (Forkhead transcription O subfamily member 3a) protects mitochondria against which lead even further protective anti-oxidizing properties. This study was designed investigate association between hyperlipidemia, intimal injury, chronic inflammation, NAD-dependent deacetylase SIRT-3, FOXO3, antioxidant genes, carotid arteries hypercholesterolemic Yucatan microswine. We found injury state led increased stress, neointimal hyperplasia, size while decreasing anti-oxidative regulatory genes mediators. The findings suggest targeting SIRT3-FOXO3aoxidative pathway will significance.

Язык: Английский

Процитировано

3

Type 1 diabetes impairs the activity of rat testicular somatic and germ cells through NRF2/NLRP3 pathway-mediated oxidative stress DOI Creative Commons
Massimo Venditti, Maria Zelinda Romano, Serena Boccella

и другие.

Frontiers in Endocrinology, Год журнала: 2024, Номер 15

Опубликована: Май 16, 2024

Background It is well known that metabolic disorders, including type 1 diabetes (T1D), are often associated with reduced male fertility, mainly increasing oxidative stress and impairing the hypothalamus–pituitary–testis (HPT) axis, consequently altered spermatogenesis sperm parameters. Herein, using a rat model of T1D obtained by treatment streptozotocin (STZ), we analyzed several parameters testicular activity. Methods A total 10 adult Wistar rats were divided into two groups five: control T1D, single intraperitoneal injection STZ. After 3 months, anesthetized sacrificed; one testis was stored at -80°C for biochemical analysis, other fixed histological immunofluorescence analysis. Results The data confirmed induced and, consequently, alterations in both somatic germ cells. This aspect highlighted enhanced apoptosis, steroidogenesis Leydig cell maturity, impaired spermatogenesis. In addition, blood–testis barrier integrity compromised, as shown levels structural proteins (N-cadherin, ZO-1, occludin, connexin 43, VANGL2) phosphorylation status regulative kinases (Src FAK). Mechanistically, dysregulation SIRT1/NRF2/MAPKs signaling pathways proven, particularly nuclear translocation NRF2, affecting its ability to induce transcription genes encoding antioxidant enzymes. Finally, stimulation inflammation pyroptosis also confirmed, increased some markers, such NF-κB NLRP3. Conclusion combined allowed us confirm has detrimental effects on Moreover, better comprehension molecular mechanisms underlying association between disorders fertility could help identify novel targets prevent treat related T1D.

Язык: Английский

Процитировано

3

A carbon dot nanozyme hydrogel enhances pulp regeneration activity by regulating oxidative stress in dental pulpitis DOI Creative Commons

Yingjuan Zhang,

Xianxian Huang,

Yicai Luo

и другие.

Journal of Nanobiotechnology, Год журнала: 2024, Номер 22(1)

Опубликована: Сен. 4, 2024

Язык: Английский

Процитировано

3

Whole organism aging: Parabiosis, inflammaging, epigenetics, and peripheral and central aging clocks. The ARS of aging DOI Creative Commons
Reinald Pamplona, Mariona Jové, José Gómez

и другие.

Experimental Gerontology, Год журнала: 2023, Номер 174, С. 112137 - 112137

Опубликована: Март 9, 2023

The strong interest shown in the study of causes aging recent decades has uncovered many mechanisms that could contribute to rate aging. These include mitochondrial ROS production, DNA modification and repair, lipid peroxidation-induced membrane fatty acid unsaturation, autophagy, telomere shortening rate, apoptosis, proteostasis, senescent cells, most likely there are others waiting be discovered. However, all these well-known work only or mainly at cellular level. Although it is known organs within a single individual do not age exactly same well-defined species longevity. Therefore, loose coordination among different cells tissues needed ensure lifespan. In this article we focus on less extracellular, systemic, whole organism level loosely coordinate keep margins its We discuss heterochronic parabiosis experiments, systemic factors distributed through vascular system like DAMPs, fragments, TF-like proteins, inflammaging, as well epigenetic proposed clocks situated levels organization from brain. interorgan systems can help determine longevity further adaptation ecosystem.

Язык: Английский

Процитировано

8

Impact of Intermittent Fasting on Metabolic Syndrome and Periodontal Disease—A Suggested Preventive Strategy to Reduce the Public Health Burden DOI Open Access
Sameena Parveen, Yaser Ali Alhazmi

International Journal of Environmental Research and Public Health, Год журнала: 2022, Номер 19(21), С. 14536 - 14536

Опубликована: Ноя. 5, 2022

Metabolic syndrome (MetS) prevalence continues to climb significantly worldwide in today’s ad libitum society. MetS has tremendous societal and economic ramifications, making it imperative develop effective strategies for preventing controlling alleviate this growing burden. Periodontal disease are associated with several risk factors. Studies the past have demonstrated that obesity, cardiovascular illness, type 2 diabetes mellitus a negative effect on severity of periodontal disease. Patients metabolic elevated serum levels proinflammatory mediators such as tumor necrosis factor-alpha interleukin-6 C-reactive protein. Similar inflammatory mediators, interleukin-6, factor-alpha, protein, increased patients severe Remarkably, intermittent fasting is underpinned by scientific evidence, claiming be most non-pharmacological, potential therapeutic alternative combating wide range metabolic, inflammatory, lifestyle-related diseases. Nonetheless, an insufficient investigation been performed determine whether benefits inflammation Here, we show interrelationship between contextualize beneficial impact modulating chronic response. We also anticipate review paves way further exploration unique research paradigm representing cost-effective strategy conventional management diseases which may serve foundation integrative vision relevant primary, diagnostic, purposes.

Язык: Английский

Процитировано

13

The mitochondrial‐endoplasmic reticulum co‐transfer in dental pulp stromal cell promotes pulp injury repair DOI Creative Commons
Xiaoyi Zhang, Chunmeng Wang, Z. Y. Zhou

и другие.

Cell Proliferation, Год журнала: 2023, Номер 57(1)

Опубликована: Июль 26, 2023

Abstract Dental pulp injury remains a clinical challenge with limited therapeutic approaches. In the present study, we sought to prove that dental stromal cells (DPSCs) mitochondrial transfer could promote repair and endoplasmic reticulum (ER)‐mitochondrial contacts have significant regulatory effect on transfer. Healthy DPSCs were co‐cultured directly or indirectly injured in first molar of 1–2 month SD rats vitro. Mitochondrial was observed after 24 h co‐culture using fluorescence microscopy live cell workstation. After for 1W, 8‐OhdG immunofluorescence, membrane potential total oxidant status/total antioxidant status used detect function before Subsequently, mitochondria‐ER co‐transfer regulated by modulating binding healthy DPSCs, results GRP78 CHOP PDI immunofluorescence haematoxylin eosin staining tissue analysed clarify effects stress (ERS), repair. Fluorescence workstation showed between DPSCs. Meanwhile, significantly restored By mitochondrial‐ER binding, efficiency affected had an impact ERS cells. promotes pulpal functional recovery damaged is binding.

Язык: Английский

Процитировано

7