Enzyme-linked Immunosorbent Assay Research Articles

Investigating the effects of 40 Hz sound stimulation on Alzheimer's disease pathways: Modulation of amyloid-β42 secretion, tau phosphorylation, phagocytosis, and autophagy.

BackgroundAlzheimer's disease (AD) is the main cause of dementia in an aging society. Previous studies have demonstrated that non-invasive light flicker and sound with gamma frequency oscillations can modulate AD-related pathology in AD mice, potentially improving patient outcomes. However, the molecular mechanism by which sound with gamma frequency oscillations inhibits the expression of amyloid-β1-42 (Aβ42) and the phosphorylation of tau, and modulating cell autophagy in nerve cells are still unclear.ObjectiveThis study aimed to explore the molecular effects of 40 Hz sound stimulation on AD-related pathways in a cellular model.MethodsWe designed a 40 Hz stimulating sound (H+ multi-frequency audio) for this study, and cells were exposed to H+ multi-frequency audio. The concentration of Aβ42 was quantified by enzyme-linked immunosorbent assay. Protein levels were examined by western blotting. Phagocytosis was examined by confocal microscopy and phagocytic analysis.ResultsFirst, we found that exposure to the 40 Hz stimulating sound inhibited the secretion of Aβ42 by activating the AβPP/ADAM10 pathway and suppressing the AβPP/BACE1 pathway. Second, 40 Hz stimulating sound inhibited tau phosphorylation at Thr181 through the inactivation of the Akt/mTOR pathway. Third, 40 Hz stimulating sound enhanced the phagocytosis and autophagy of Aβ42 through the AMPK/ULK/LC3B pathway in cells.ConclusionsOur study showed that 40 Hz stimulating sound is involved in the inhibition of Aβ42 secretion, p-Tau protein expression, and the promotion of phagocytosis and Aβ42 autophagy in cells. We suggest that 40 Hz stimulating sound could be a potential intervention to attenuate AD progression in the future.

Assessment of Serum Cytokine Levels in Keratoconus Patients.

Background: While keratoconus (KC) has traditionally been classified as a non-inflammatory corneal disorder, emerging evidence suggests that inflammatory processes may be involved in its pathogenesis. This study investigated whether systemic inflammation contributes to KC development by measuring serum levels of key pro-inflammatory cytokines in KC patients compared to healthy controls. Methods: This cross-sectional comparative study included 60 participants aged 18-30 and was divided into three equal groups: healthy controls, progressive KC, and stable KC. The levels of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and interleukin-1 beta (IL-1β) in the serum were measured through an enzyme-linked immunosorbent assay. KC severity was classified based on mean keratometry values. Results: There were no significant differences detected in serum IL-6, TNF-α, and IL-1β levels across groups (p > 0.05). Moreover, no significant correlations were found between systemic cytokine levels and KC severity categories (p > 0.05). Conclusions: Systemic levels of IL-1β, IL-6, and TNF-α do not significantly differ between KC patients and controls nor do they correlate with disease severity, reinforcing the hypothesis that KC involves primarily local inflammatory processes.

Traditional Chinese medicine Youguiyin decoction ameliorate glucocorticoid-induced osteonecrosis in rat by modulating ROS/PHD2/HIF-1α oxidative stress signaling pathway in bone marrow mesenchymal stem cells

BackgroundThe incidence of osteonecrosis is increasing annually due to the widespread use of glucocorticoids. Recent evidence suggests a significant association between glucocorticoid-induced osteonecrosis and oxidative stress. Youguiyin (YGY) decoction, a classic formula of traditional Chinese medicine, has been widely used for the prevention of glucocorticoid-induced osteonecrosis. However, its underlying pharmacological mechanisms are still not fully understood.MethodsUPLC-Q-TOF–MS and network pharmacology were used to elucidate the material basis of YGY decoction and its mechanism for the treatment of glucocorticoid-induced osteonecrosis. The anti-oxidative stress and bone-enhancing effects in vivo were detected by hematoxylin–eosin (HE) staining, serum metabolomics, enzyme-linked immunosorbent assay (ELISA), immunohistochemistry (IHC), and Western Blot (WB). Rat bone marrow mesenchymal stem cells (BMSCs) were induced with dexamethasone (DXMS) for 24 h, followed by YGY medicated serum for 24 h. Significantly up- and down-regulated genes were detected by RNA sequencing. Oxidative stress levels were detected by ROS fluorescence. Alizarin red S staining was used to detect osteogenic effects. WB and ELISA were used to detect the expression of proteins related to the ROS/PHD2/HIF-1a pathway.ResultsThe application of YGY decoction significantly promoted bone repair and antagonized excess reactive oxygen species (ROS) generation in glucocorticoid-associated osteonecrosis of the femoral head (GA-ONFH) rats. In addition, YGY medicated serum antagonized DXMS-induced ROS production and promoted osteogenic differentiation in BMSCs. We also found that YGY medicated serum attenuated excess ROS generation while PHD2 expression was significantly increased, HIF-1α expression was significantly decreased and RUNX2 expression was significantly increased.ConclusionThese results provide compelling in vivo and in vitro evidence that YGY decoction may play a role in promoting glucocorticoid-induced osteonecrosis bone repair by targeting the mediation of the ROS/PHD2/HIF-1α oxidative stress signaling pathway, thus providing a new theoretical basis for the clinical application of YGY decoction to glucocorticoid-induced osteonecrosis.Graphical

Investigating the Therapeutic Potential of Crude Leech Saliva Based on Its Anticancer, Antioxidant, and Anti-Inflammatory Effects

Leech therapy is a biotherapeutic approach that has been traditionally used for centuries and is currently being re-evaluated in modern medicine. The efficacy of this treatment is attributed to various bioactive compounds found in leech saliva, which exhibit anticoagulant, anti-inflammatory, antioxidant, and anticancer properties. It has been demonstrated that leech saliva possesses the potential to modulate inflammatory processes and apoptotic mechanisms. In this study, the therapeutic potential of the saliva of Hirudo verbana was evaluated, and its biological and pharmacological effects were comprehensively investigated. The anticancer effects, antioxidant capacity, and anti-inflammatory activity of the crude leech saliva were assessed using human umbilical vein endothelial cells and epithelial ovarian cancer cells. The chemical composition of the saliva was analyzed using gas chromatography–mass spectrometry, while the protein content was determined by the Bradford assay. Antioxidant activity was measured using the 2,2-diphenyl-1-picrylhydrazyl radical scavenging assay, inflammatory effects were evaluated by Enzyme-Linked ImmunoSorbent Assay, and cell viability was determined using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. The findings revealed that crude leech saliva had a minimal effect on healthy cells but showed a selective effect on the viability of ovarian cancer cells. At low concentrations (3.13%), 99.16% of healthy cells remained viable, whereas this rate decreased to 89.25% in cancer cells; at high concentrations (50%), cell viability in cancer cells declined to 63.02%. Gas chromatography–mass spectrometry analysis identified compounds such as gibberellic acid and 6-[(4-methoxyphenyl)methoxy]-4,4,5,7,8-pentamethyl-3H-chromen-2-one, which demonstrated high affinity for the antiapoptotic proteins Bcl-2 and Survivin in molecular docking analyses. In conclusion, the crude leech saliva was confirmed to possess anti-inflammatory, antioxidant, and anticancer properties. However, further biochemical and clinical research is needed to elucidate the underlying mechanisms of these biological effects in greater detail.

Obacunone acts as a histone deacetylase 1 inhibitor to limit p38MAPK signaling and alleviate osteoarthritis progression

BackgroundOsteoarthritis (OA) is an age-related progressive degenerative disorder characterized by cartilage extracellular matrix degradation and inflammation. In this study, we explored the function and mechanism of action of obacunone (OB) in inhibiting OA progression.MethodsThe degradation of articular cartilage and its severity were examined using Safranin O-fast green and hematoxylin and eosin (HE) staining. Chondrocyte survival was evaluated using a cell counting kit-8 assay. In addition, qRT-PCR, western blot analysis, immunohistochemical staining, and enzyme-linked immunosorbent assay were performed to evaluate the effects of OB on cartilage injury.ResultsOB mitigated cartilage lesions in rats with anterior cruciate ligament transaction-induced OA. The protein expression of collagen II was increased and the protein expression of ADAM metallopeptidase with thrombospondin type 1 motif 5 (ADAMTS-5), matrix metalloproteinase (MMP)-13, and RUNX family transcription factor 2 (RUNX2) was reduced in the articular cartilage of OB-treated rats. Moreover, OB exhibited anti-inflammatory activities by reducing the serum levels of interleukin (IL)-6, tumor necrosis factor (TNF)-α, IL-1β, and IL-18. In IL-1β-stimulated primary chondrocytes, OB dose-dependently elevated the expression of collagen II, and decreased the expression of ADAMTS-5, MMP-13, RUNX2 and inflammatory cytokines. Histone deacetylase 1 (HDAC1) was identified as a predicted OB target. OB inhibited HDAC1 expression to limit the activation of p38MAPK signaling. The transfection of chondrocytes with HDAC1 or p38MAPK overexpression plasmids reversed the chondroprotective effects of OB.ConclusionOB mitigated OA progression by binding to HDAC1 and inhibiting p38MAPK signaling, indicating that OB may be a promising drug for the treatment of OA.

Aerobic Exercise and Celastrol: A Promising Combination for Achilles Tendon Regeneration

Background: Tendons are subjected to mechanical stress and strain during daily activities and physical exercise, which makes them susceptible to injury. Objectives: This randomized trial evaluated the effects of a 4-week combination of training and celastrol on the healing of Achilles tendon ruptures in rats. It assessed cytokine levels, gene expression, and histological changes. Methods: Rats with Achilles tendon ruptures were randomly assigned to several treatment groups: Sham, negative control, training, celastrol, and a combination of training and celastrol. Eligibility criteria included age, weight, and the absence of pre-existing tendon injuries. The assessments included enzyme-linked immunosorbent assay (ELISA) to measure cytokine levels [bFGF, IGF1, cyclooxygenase 2 (COX2)], real-time polymerase chain reaction (RT-PCR) to analyze gene expression (scleraxis, periostin, MMP9, collagen I), and histological analysis using Masson's trichrome staining to evaluate collagen organization. Results: The training-celastrol group exhibited the highest levels of bFGF, IGF1, and COX2, indicating a synergistic effect on tendon healing compared to the sham and negative control groups, with effect sizes of 0.85 (95% CI: 0.70 - 1.00). Additionally, RT-PCR results showed that the training-celastrol group had the highest expression of scleraxis, periostin, MMP9, and collagen I, suggesting enhanced tendon repair and remodeling. Histological analysis revealed that the training-celastrol group displayed the most organized collagen fibers, whereas the sham group showed regular organization, and the negative control group exhibited disorganized fibers. Conclusions: The study concluded that combining aerobic training and celastrol significantly enhances tendon healing by improving cytokine levels, gene expression, and collagen organization. Outcome measures were assessed at baseline, mid-treatment (week 2), and post-treatment (week 4) to evaluate temporal changes. These findings highlight the effectiveness of these therapeutic strategies in promoting tendon repair and maintaining structural integrity.

The role of complement C1q in atrial fibrillation: a marker for disease progression and surgical outcomes

Background and objectiveThe complement system plays a crucial role in the pathogenesis and progression of cardiovascular diseases. C1q, a key initiator of the classical pathway, is closely associated with various chronic inflammatory conditions. This observational study aims to elucidate the potential risk relationship between serum complement C1q levels and atrial fibrillation (AF).Materials and methodsThis retrospective cohort study included 812 AF patients treated at the Affiliated Hospital of Qingdao University from January 2020 to October 2022, comprising 694 patients in the paroxysmal AF group and 118 in the persistent AF group. Serum complement C1q levels were measured using an enzyme-linked immunosorbent assay (ELISA).ResultsSerum C1q levels in the AF group were significantly lower than those in the control group (P < 0.001). Logistic regression analysis indicated that reduced plasma C1q levels were independently associated with the incidence of AF (95% CI = 0.974–0.981, P = 0.001). Additionally, ROC curve analysis confirmed the close association between plasma C1q levels and AF, highlighting the predictive value of C1q for AF. Further investigation revealed that C1q serves as an independent risk factor for complex fractionated atrial electrograms (CFAE) in the superior left atrium of paroxysmal AF patients (95% CI = 0.984–0.998, P = 0.031), suggesting its potential as a clinical indicator for guiding AF surgical interventions.ConclusionSerum C1q levels are significantly reduced in patients with AF. The presence of CFAE in the superior left atrium of paroxysmal AF patients may be potentially associated with C1q levels. Low complement levels are associated with atrial fibrillation compared to individuals without AF and may represent a potential underlying cause of impaired sinus rhythm maintenance following pulmonary vein isolation. Complement C1q may play a critical role in the pathogenesis of AF.

Higher Hepatitis E Seroprevalence in Workers in the Pig Sector in Flanders, Belgium: Results From a Seroprevalence Case-Control Study.

Autochthonous hepatitis E virus (HEV) infection in industrialised countries is a zoonosis. Pigs are recognised as the principal reservoir. Consequently, workers in the pig sector may be a high-risk occupational group for HEV infection. The current study aims to investigate whether workers exposed to pigs or pork have a higher seroprevalence of HEV IgG in comparison to a control group. A cross-sectional study was conducted involving 92 individuals occupationally exposed to pigs or pork and 217 control subjects outside the pig sector. Socio-demographic variables, information about occupation, and a number of relevant confounding variables (such as eating habits, and history of blood transfusions) were gathered by a questionnaire. Serum samples were tested for anti-HEV IgG antibodies using an enzyme-linked immunosorbent assay (ELISA). Our study revealed a significantly higher seroprevalence of HEV antibodies in pig workers (32.6%) compared to the control group (9.2%) (p < 0.001). The relation between occupational exposure and HEV seropositivity remained significant in the multiple logistic regression analysis, in which the odds were adjusted for age, gender, and eating habits. The results from this first HEV IgG serology study in the pig sector in Belgium demonstrate that workers in this sector have a higher risk for HEV infection compared to a population not occupationally exposed to pigs and pork. These findings underscore the need for targeted occupational health interventions, including improved hygiene practices and informing employees with risk profiles, to mitigate the risk of HEV infection among pig workers.

Extracellular vesicles therapy alleviates cisplatin-ınduced testicular tissue toxicity in a rat model.

Cisplatin is a commonly used chemotherapy agent effective against various cancers, however it induces significant gonadotoxicity and infertility due to its adverse effects on testicular function. The underlying mechanisms of cisplatin-induced testicular damage include oxidative stress and dysregulated autophagy. This study investigates the potential of extracellular vesicles (EVs) to mitigate cisplatin-induced testicular damage through their regenerative, antioxidant, and autophagy-modulating properties. In the testicular toxicity model, thirty-two male rats were randomly divided into four groups (n = 8): control, EVs-only, Cis-only, and Cis + EVs. A single intraperitoneal dose of 7.5mg/kg cisplatin was administered on the first day. On the six day, the EVs treatment group received a single dose of EVs (8x107/100μl) intravenously. Animals were sacrificed on day eight. Testicular histoarchitecture was assessed via hematoxylin and eosin staining. Sperm parameters, including motility and count, were measured using light microscopy. Hormone levels (testosterone and inhibin) were determined via enzyme-linked immunosorbent assay (ELISA). Oxidative stress markers, such as glutathione peroxidase (GSH-PX), superoxide dismutase (SOD), catalase (CAT), and is a metabolite malondialdehyde (MDA), were quantified using colorimetric assays. Autophagy and steroidogenesis were evaluated through immunohistochemical analysis of Beclin-1, p62, LC3-2, SF-1, and StAR. Cisplatin exposure caused significant testicular damage, characterized by reduced germinal epithelium and degeneration of seminiferous tubules (p < 0.001). These structural changes led to hormonal imbalances, as evidenced by declines in testosterone (p < 0.005) and inhibin (p < 0.001). Additionally, sperm motility (p < 0.05) and count (p < 0.001) were adversely affected. Immunohistochemical analysis revealed upregulation of autophagy markers (p < 0.001), indicating heightened autophagic activity, alongside downregulation of steroidogenic factors (p < 0.001), which contributed to impaired steroidogenesis. Elevated levels of malondialdehyde (MDA) (p < 0.01) and decreased activities of antioxidant enzymes-GSH-PX, SOD, and CAT (p < 0.001) pointed to increased oxidative stress as a contributing mechanism. In contrast, treatment with extracellular vesicles (EVs) significantly improved testicular histoarchitecture (p < 0.001) and restored hormonal levels toward normal (testosterone p < 0.005, inhibin p < 0.001). Furthermore, EVs reduced the expression of autophagy markers (p < 0.001) and enhanced the levels of steroidogenic factors (p < 0.05). Notably, MDA levels decreased (p < 0.001), while antioxidant activities increased (p < 0.001), suggesting a protective effect of EVs against oxidative stress. EVs protect against cisplatin-induced reproductive toxicity by modulating oxidative stress and autophagy pathways, preserving testicular function and fertility. These findings suggest that EVs may be a promising therapeutic strategy for mitigating cisplatin's negative effects on reproductive health. Further exploration of dosing regimens and localized applications is recommended for improved efficacy.

Inverted day-night feeding during pregnancy affects the brain health of both maternal and fetal brains through increasing inflammation levels associated with dysbiosis of the gut microbiome in rats

BackgroundIn both humans and rodents, inappropriate feeding times during pregnancy can cause maternal metabolic abnormalities, increasing the risk of neurodevelopmental disorders in both the mother and offspring. Using a rat model, this study investigates whether feeding only during the inactive phase in rats leads to anxiety-like behaviors and abnormal brain development in fetuses through gut microbiota imbalance.Methods10-week-old female rats in the inactive-phase feeding group (IF group) were first trained for daytime feeding, ensuring that energy intake was statistically insignificant and different from that of the normal diet feeding group (ND group). They were then paired with male rats, and the previous feeding regimen was continued after pregnancy. Anxiety-like behavior was evaluated using the open-field test. Maternal caecal microbiota was analyzed using 16S rRNA sequencing. Enzyme-linked immunosorbent assay (ELISA) measured serum inflammation factors. RT-PCR was employed to assess mRNA levels of integrity genes and inflammatory cytokines in the maternal hippocampi, intestines, fetal brains, and placentae.ResultsThere were no statistically significant differences in energy intake or body weight gain between the IF and ND groups. In the open field test, dams in the IF group exhibited anxiety-like behavior, as indicated by fewer entries into and shorter duration in the central zone. Active-phase fasting elevated maternal serum inflammatory cytokine levels and impaired antioxidant capacity. It also increased intestinal permeability and induced gut microbiota dysbiosis, characterized by a decrease in Akkermansia and an increase in Dubosiella. Changes in the expression of intestinal circadian genes and elevated intestinal inflammatory cytokines were observed. Lipopolysaccharide (LPS) translocated into the maternal circulation, activated Toll-like receptor 4 (TLR 4), and passed through the compromised placental barrier into the fetal brain, leading to increased expression of inflammatory cytokines in the fetal brain.ConclusionsThe misalignment between maternal feeding time and the biological clock during pregnancy disrupts the balance of the gut microbiota and peripheral rhythms. The impaired intestinal and placental barriers allow LPS from the gut to infiltrate the maternal hippocampus and fetal brain, increasing inflammation and impacting both maternal and fetal brain health.

Surrogate Markers of Intestinal Permeability, Bacterial Translocation and Gut-Vascular Barrier Damage Across Stages of Cirrhosis.

Portal hypertension, gut barrier dysfunction, and pathological bacterial translocation are hallmarks of cirrhosis driving complications. As measuring gut barrier function is demanding, surrogate markers have been proposed, but their intercorrelation and applicability across different stages of advanced liver disease, particularly in acute-on-chronic liver failure (ACLF), are largely unknown. Proposed markers of gut barrier dysfunction and bacterial translocation were quantified in sera from 160 patients with cirrhosis across different disease stages of compensated and decompensated cirrhosis as well as from 20 patients in hepatic and portal vein serum before and after the insertion of transjugular intrahepatic portosystemic stent (TIPS) using enzyme-linked immunosorbent assay (ELISA). Across all stages of liver disease, the gut-vascular barrier (GVB) marker plasmalemma vesicle protein-1 (PV-1) correlated with bacterial translocation markers endogenous endotoxin-core IgA antibodies (EndoCAb) and LPS-binding protein (LBP) but not with intestinal damage markers intestinal fatty acid binding protein (I-FABP) and zonulin-family peptides (ZFP). PV-1 and EndoCAb were higher in decompensated cirrhosis without further increase in ACLF. Among investigated markers, only I-FABP correlated with the portosystemic pressure gradient, and TIPS insertion significantly reduced portal concentrations within 24 h. Higher PV-1 levels indicated poor transplant-free survival in univariate and multivariable analysis. Surrogate markers of bacterial gut barrier dysfunction and bacterial translocation like ZFP, LBP and EndoCAb appear of limited use in advanced stages of cirrhosis and are confounded by hepatic synthesis capacity, portal congestion and acute phase responses. The prognostic implications of circulating PV-1 in decompensated cirrhosis levels demand further investigation.

Characterization and Isolation of Ginger Phenols from Zingiber officinale Rhizomes through in Silico-Based Reverse Annotation and Molecular Networking.

Ginger is a rich source of ginger phenols with an anti-inflammatory property. Antineuroinflammatory pathways represent a promising therapeutic strategy for neurodegenerative diseases. Ginger was selected as our research object to discover bioactive constituents responsible for the antineuroinflammatory effect. An in silico-based reverse annotation strategy, in conjunction with molecular networking, was employed for the large-scale annotation of ginger phenols from ginger. A total of 174 ginger phenols and 235 ginger phenol dimers were annotated. Five new ginger phenols (1-5) and 18 known ginger phenols (6-23) were isolated following this proposed strategy, among which compound 1 was a new natural product and compounds 2-3 were novel ginger phenol dimers. Their structures were elucidated using extensive spectroscopic data and semisynthesis methods. Compounds 2, 8, 12, 18, and 19 exhibited a capacity to inhibit nitric oxide (NO) production and demonstrated antineuroinflammatory activity in lipopolysaccharide (LPS)-induced BV2 cells at the concentrations of 10, 20, and 40 μM. Enzyme-linked immunosorbent assay (ELISA) showed that compounds 2, 18, and 19 could significantly reduce the expression levels of cyclooxygenase-2 (COX-2) and interleukin-1β (IL-1β). In addition, compounds 2 and 18 displayed a certain inhibitory effect on the expressions of interleukin-10 (IL-10) and interleukin-6 (IL-6). The Western blot analysis revealed that compounds 18 and 19 effectively attenuated the expression of IL-1β, while only compound 2 inhibited the expression of phosphorylated nuclear factor kappa B (p-NF-κB) in BV2 cells. This study demonstrates the great potential and prospect of the proposed strategy in the utilization of ginger resources. Additionally, it reveals that ginger contains diverse ginger phenols with antineuroinflammation activity.

Ventriculoscopy combined with Ommaya reservoir implantation for treatment of hydrocephalus with atypical neuroimaging features of neurocysticercosis: A case report.

Cysticercosis-induced hydrocephalus presents diagnostic and therapeutic challenges owing to its heterogeneous clinical manifestations. Acute hydrocephalus secondary to parasitic infections of the central nervous system (CNS) requires tailored surgical interventions to address impaired cerebrospinal fluid (CSF) dynamics and intracranial hypertension. A 27-year-old male reported intermittent dizziness and headaches persisting for 3 years and a recent onset of vomiting over the past month. Neuroimaging demonstrated ventricular enlargement, thickened basal membranes, and elevated intracranial pressure, without classical cysticercosis imaging markers. Serological and CSF enzyme-linked immunosorbent assay (ELISA) tests confirmed the presence of antibodies against cysticercosis. The patient was diagnosed with acute exacerbation of chronic hydrocephalus secondary to a CNS cysticercosis infection complicated by extensive ependymitis and CSF absorption dysfunction. Ventriculoscopy identified impaired CSF circulation caused by ependymitis, precluding conventional ventriculoperitoneal (V-P) shunts or endoscopic third ventriculostomy. An Ommaya reservoir was implanted to regulate intracranial pressure, which was supplemented by antiparasitic therapy with praziquantel. Postoperative follow-up confirmed resolution of hydrocephalus and complete alleviation of neurological symptoms, with no complications observed. This case highlights ventriculoscopy-guided Ommaya reservoir implantation as a safe and effective alternative for managing parasitic infection-induced hydrocephalus when standard surgical options are contraindicated. This strategy addresses both CSF dynamics and infection and provides a reference for managing atypical neurocysticercosis cases.

Treatment of Premature Ovarian Failure Mouse Model Using Granulosa-Like Cells Derived from Wharton's Jelly-Mesenchymal Stem Cells.

Premature ovarian failure (POF) is a significant reproductive disorder characterized by the loss of ovarian function, leading to infertility and endocrine disruption. Hormone replacement therapy (HRT) remains the most commonly used clinical treatment for POF. However, in patients with a history of ovarian or breast cancer, HRT poses significant risks, necessitating the development of alternative approaches. Stem cell-based therapy has emerged as a promising option for treating female infertility disorders such as POF. This study aimed to evaluate the therapeutic effects of ovarian granulosa-like cells (OGLCs) derived from Wharton's jelly-mesenchymal stem cells (WJ-MSCs) in a POF mouse model. WJ-MSCs were successfully differentiated into OGLCs using combination with a growth factor cocktails, as confirmed by the significant upregulation of granulosa cell-specific markers (P < 0.01). To assess their therapeutic potential, POF was induced in female mice using cyclophosphamide and busulfan, and OGLCs were injected into the ovaries. After 3 weeks, vaginal smear analysis revealed restoration of estrus cycle in OGLC-treated mice. Enzyme-linked immunosorbent assay analysis demonstrated the recovery of serum 17β-estradiol and follicle-stimulating hormone levels (P < 0.05), while histological staining confirmed increased follicular development and restoration of ovarian structure. Furthermore, real-time quantitative polymerase chain reaction analysis showed a significant upregulation of genes related to follicular development and primordial follicle activation, including downstream molecules of the mTOR/PI3K pathway, following OGLCs treatment. These findings suggest that OGLCs possess a strong potential for restoring ovarian function in POF. This study provides evidence supporting the use of OGLCs as a novel cell-based therapeutic approach for female reproductive diseases.

A deeper evaluation of cytokeratin fragment 21-1 as a lung cancer tumor marker and comparison of different assays.

A deeper evaluation of cytokeratin fragment 21-1 as a lung cancer tumor marker and comparison of different assays.

Anti-annexin A4 antibody as a biomarker for desquamative interstitial pneumonia.

Anti-annexin A4 antibody as a biomarker for desquamative interstitial pneumonia.

Design of hybrid aptamer-molecularly imprinted polymer nanoparticles for selective binding of oxidized low-density lipoprotein in an ELISA-mimic system.

Design of hybrid aptamer-molecularly imprinted polymer nanoparticles for selective binding of oxidized low-density lipoprotein in an ELISA-mimic system.

Anti-TFAM antibodies link mitochondrial damage with antiphospholipid syndrome and thrombosis in SLE.

Anti-TFAM antibodies link mitochondrial damage with antiphospholipid syndrome and thrombosis in SLE.

Chimeric Recombinant Protein (rErpY-LemA) as Innovative Tools for Animal Leptospirosis Serodiagnosis.

Chimeric Recombinant Protein (rErpY-LemA) as Innovative Tools for Animal Leptospirosis Serodiagnosis.

IgG antibody response to Mycobacterium tuberculosis curli pili (MTP) in people from different geographical regions in Sub-Saharan Africa.

IgG antibody response to Mycobacterium tuberculosis curli pili (MTP) in people from different geographical regions in Sub-Saharan Africa.