Nitric oxide (NO) plays pivotal roles in numerous physiological and pathological processes, making its real-time detection in biological systems of paramount importance. Herein, a novel quinoline-based fluorescent probe (KL) was developed for the sensitive and selective detection of NO in vitro and in vivo. The probe achieves NO sensing through a unique NO-induced cyclization-responsive mechanism. Upon reaction with NO, the thiocarbohydrazide moiety of KL undergoes specific cyclization to form a 1,2,3,4-thiatriazole ring, leading to a distinct red shift in its UV-vis absorption spectrum and pronounced fluorescence quenching at 550 nm. Probe KL exhibits a rapid response time (40 s), a low detection limit (78 nM), excellent selectivity, and a large Stokes shift (150 nm). Benefiting from its favorable biocompatibility, probe KL has been successfully applied for the visualization of NO in living HeLa cells. Furthermore, probe KL was successfully extended to real-time fluorescence imaging of NO in live nude mice. Consequently, the development of probe KL would provide a novel approach for further elucidating the physiological functions of NO in biological systems and a new cyclization reaction-based responsive strategy for NO detection.

Intestinal ischemia-reperfusion (IIR) injury can cause intestinal barrier damage, systemic inflammatory response, and high mortality. The key mechanism is the disorder of the mitochondrial-endoplasmic reticulum network. Ubiquitin-specific peptidase 30 (USP30), located on the outer mitochondrial membrane, can reverse the partial ubiquitination of Parkin substrates or completely remove the ubiquitin chain to maintain mitochondrial function. Mitofusin 2 (MFN2) is a mitochondrial outer membrane fusion protein that mediates mitophagy and endoplasmic reticulum stress and participates in the formation of mitochondria-associated endoplasmic reticulum (MAMs). Our research showed that IIR reduces the protein expression of USP30 and MFN2, and overexpression of USP30 can increase the stability of MFN2 through deubiquitination and alleviate the damage caused by IIR. After overexpression of MFN2, mitochondrial dysfunction and endoplasmic reticulum stress caused by IIR are restored, while knockdown of MFN2 weakens the protective effect of USP30 on the MAMs. USP30 alleviates endoplasmic reticulum stress and mitochondrial dysfunction caused by intestinal ischemia-reperfusion injury by reducing the ubiquitination level of MFN2. The regulation of USP30 may be a promising strategy for alleviating intestinal ischemia-reperfusion injury.

Protein fatty acylation encompasses S/N/O-acylation modifications that regulate diverse cellular functions, yet current methods cannot simultaneously capture all three types. Here, we present a dual-identification strategy that integrates metabolic labeling with click chemistry, hydroxylamine mediated selective hydrolysis, and cleavable bioorthogonal probes for comprehensive fatty acylation site detection. Using Alk-C16:0 and Alk-C18:0 probes in HepG2 cells, we identified 1,310 and 1,131 total fatty acylation sites respectively, including 588 and 674 S-acylation sites substantially exceeding single method coverage. Integration of open and closed searches revealed probe intracellular conversion induced acyl chain heterogeneity, improving identification accuracy. We discovered diagnostic ions revealing acyl chain structure and N-acylation specific cyclic immonium ions that discriminate between modification subtypes. This strategy enables unprecedented comprehensive protein fatty acylation characterization, providing a robust platform for investigating molecular mechanisms of these essential modifications.

Bisulfite (HSO3−) is widely employed as a preservative and bleaching additive in food processing. As a key sulfur dioxide (SO2) derivative, it participates in multiple physiological processes. Nevertheless, excessive exposure or abnormal accumulation of HSO3− can threaten human health, making the selective and sensitive detection of HSO3− in food, environmental, and biological samples highly necessary. Herein, a novel red-emitting fluorescent probe (FSQ) is reported for the specific recognition of HSO3−via an unprecedented sensing mechanism. Relying on the ICT effect, FSQ displays strong red fluorescence at 640 nm. The specific 1,4-nucleophilic addition between the 2H-chromen-2-imine moiety of FSQ and HSO3− can effectively interrupt the ICT process and trigger remarkable fluorescence quenching. FSQ displays excellent selectivity, high sensitivity (7.38 μM) and broad pH adaptability. The quantitative detection of HSO3− in real food sample was successfully realized via FSQ. Furthermore, the smartphone-assisted test strip platform based on FSQ was fabricated for rapid, quantitative and on-site analysis of HSO3−. Importantly, FSQ exhibits low cytotoxicity and favorable biocompatibility, enabling it to effectively track HSO3− levels in both HeLa cells and nude mice. This study not only provides a reliable tool for food safety supervision, environmental safety assessment and investigating the pathophysiological roles of HSO3−, but also presents a new design strategy for developing HSO3−-selective fluorescent probes.

Sulfur dioxide (SO2) and its derivative, bisulfite (HSO3-), are widely used in daily life and play indispensable roles in physiological regulation. However, aberrant fluctuations or excessive intake of HSO3- can pose multiple threats to human health. Consequently, the sensitive and specific detection of HSO3- is of critical importance. Herein, a near-infrared (NIR) fluorescent probe XDS2 for HSO3- detection was developed by expanding pi-conjugation system and enhancing electron-donating ability. Owing to the intramolecular charge transfer (ICT) effect, XDS2 exhibits strong NIR emission at 740 nm with a large stokes shift of 193 nm. XDS2 shows a good linear response within the HSO3- concentration range of 0-100 mu M, with a detection limit of 6.56 mu M. XDS2 was applied to the quantitative detection of HSO3- in food samples, and rapid on-site quantitative determination of HSO3- was achieved via a smartphone-assisted XDS2-based test-strip platform. Furthermore, fluorescence imaging of HSO3- in living cells and mice was successfully demonstrated using XDS2. The developtment of XDS2 not only offers a new approach for highly sensitive detection and imaging of HSO3-, but also provides an important theoretical foundation for the molecular design of high-performance NIR fluorescent probes.

Carbon monoxide (CO) functions as a critical signaling molecule in both mammalian inflammation and plant stress responses. However, existing techniques face challenges in real-time monitoring of CO dynamics across biological kingdoms. Here we developed Z2CO, a xanthene-based red-emitting fluorescent probe constructed on a Pd(0)-triggered Tsuji-Trost allylic cleavage mechanism. Upon CO recognition, Z2CO generates a distinct turn-on fluorescence signal at 625 nm within 10 min. The probe exhibits favorable properties including an 80 nm Stokes shift, low detection limit (0.193 μM, 3σ/k criterion), excellent water solubility, and minimal cytotoxicity, making it suitable for complex biological applications. Using Z2CO, we successfully visualized endogenous CO generation in pulmonary tissues of lipopolysaccharide-induced bacterial pneumonia mice and quantitatively evaluated anti-inflammatory drug efficacy. Furthermore, we extended Z2CO to plant systems, achieving real-time monitoring of CO dynamics in cadmium-stressed edible sprouts and brassica rapa. These investigations provide direct evidence for CO involvement in heavy metal-triggered signal transduction networks. Collectively, Z2CO constitutes a versatile tool for elucidating CO-mediated physiological and pathological processes across animal and plant systems.

Osteosarcoma (OS) is a malignant neoplasm arising from bone tissue. The OS exhibited a significant degree of heterogeneity, with a high incidence of local invasion and a high rate of metastasis. Approximately 25% of those diagnosed with OS present with metastases, with the lungs being the most prevalent site, followed by the bones or lymph nodes. The 5-year survival rate for patients with OS with lung metastasis is only 10% to 30%. Adjuvant chemotherapy regimens significantly enhanced the 5-year survival rate in patients diagnosed with non-metastatic OS. However, the same regimens did not provide a substantial improvement in survival for patients with OS who had acquired lung metastasis or had recurrence. Moreover, the extensive use of chemotherapy medications often results in the development of resistance to chemotherapy in patients with OS, which frequently culminates in treatment ineffectiveness. Natural products (NPs) are significant reservoirs of anti-cancer medications. Preclinical investigations have shown that certain NPs had substantial promise for treating OS. However, there is currently a lack of a comprehensive overview of the use of NPs in OS treatment. In this review, we provide a comprehensive overview of the NPs, which include polyphenols, alkaloids, and terpenoids, that have the potential to be effective in the treatment of OS.

The integration of precise bacterial detection with effective sterilization, while mitigating the risk of bacterial resistance, is of paramount importance in clinical medicine and public health. Herein, we present a novel aggregation-induced emission (AIE) fluorescent probe, PTZ-PD, engineered for the simultaneous detection and eradication of bacteria in animal models. PTZ-PD features a donor-acceptor (D-A) architecture composed of a phenothiazine donor and a quinoline propionitrile acceptor, which endows the probe with long-wavelength emission (λem ≈ 680 nm) and remarkable AIE characteristics, enabling quantitative detection of bacteria. The probe exhibited high sensitivity, achieving detection limits (LOD) of 1.01 × 103 CFU/mL for Staphylococcus aureus (S. aureus) and 2.28 × 103 CFU/mL for Escherichia coli (E. coli) within 1 min. Furthermore, PTZ-PD demonstrated potent light-activated antibacterial activity, achieving inhibition rates of 98.3% against S. aureus and 92.7% against E. coli after only 30 min of sunlight irradiation. Mechanistic studies using reactive oxygen species (ROS)-sensitive fluorescent probes revealed that the bactericidal effect is mediated by light-induced ROS generation. The fluorescence of the probe was also responsive to environmental viscosity. Importantly, in a murine wound infection model, PTZ-PD effectively promoted healing and demonstrated excellent biosafety. This work not only enriches the toolbox of AIE-based theragnostic agents but also provides a promising candidate for combating bacterial infections and informing future drug development.

Following the publication of the above article, an interested reader drew to the authors' attention that, concerning the Masson trichrome‑stained sections of left ventricles shown in Fig. 6A on p. 395, a portion of the panel representing the DM+EGCG group (centre panel) contained an overlapping area with a portion of the panel from the DM group (second panel on the left), which was representative of the experiment that lacked EGCG treatment. Upon investigating this figure, the authors have realized that the affected data panels were inadvertently assembled incorrectly. This error arose due to an oversight in image selection made during figure assembly. A revised version of Fig. 6, now showing the correct data panel for the DM+EGCG group (centre panel) in Fig. 6A, is shown on the next page. Also note that the published version of Fig. 6A did not feature labels portraying the different experimental groups in this figure part, and these are now included in the revised figure to improve its clarity. The authors confirm that the error associated with this figure did not have any significant impact on either the results or the conclusions reported in this study, and all the authors agree with the publication of this Corrigendum. The authors are grateful to the Editor of International Journal of Molecular Medicine for allowing them the opportunity to publish this Corrigendum; furthermore, they apologize to the readership of the Journal for any inconvenience caused. [International Journal of Molecular Medicine 40: 389‑399, 2017; DOI: 10.3892/ijmm.2017.3014].

Background Glutathione (GSH), as the most abundant intracellular biothiol, plays pivotal roles in maintaining redox homeostasis and regulating cellular functions. Abnormal GSH levels are closely associated with various pathological states, including cancer, neurodegenerative diseases, and oxidative stress-related disorders. However, accurately monitoring GSH dynamics in complex biological systems remains challenging due to the limitations of single-modal imaging techniques, which often lack either sufficient sensitivity or adequate spatial resolution and tissue penetration. In this context, fluorescent/magnetic resonance (MR) dual-modal imaging has emerged as a powerful approach, enabling simultaneous acquisition of high-resolution anatomical structures and highly sensitive functional information. Results This study reports a novel fluorescent/magnetic resonance (MR) dual-modal probe, RG, for detecting GSH. The probe synergizes the high sensitivity of fluorescence imaging with the deep-tissue penetration of MR imaging, overcoming the limitations of single-modal methods. In the presence of GSH, a nucleophilic reaction triggers rhodamine spirolactam ring-opening, releasing the fluorophore. Concurrently, the gadolinium complex coordinates an additional water molecule, markedly increasing its longitudinal relaxivity (r1), thus enabling synchronous dual-signal activation. Probe RG exhibits high stability, specificity for GSH, a rapid response (5 ms), physiological pH compatibility, and low cytotoxicity, achieving a detection limit of 2.47 μM. Ultimately, probe RG was successfully applied for fluorescence and magnetic resonance dual-modal imaging of GSH in a mouse model. Significance This success provides not only a reliable means to track GSH in real time but also a generalizable design strategy for dual-modal probes, advancing our capacity to decipher GSH-related biology and disease mechanisms.

β-hydroxybutyric acid (BHB), a key ketone body with energy substrate and epigenetic regulatory roles, has contradictory effects in pathological contexts. Intestinal ischemia-reperfusion (IIR) is a life threatening perioperative complication characterized by metabolic disorders and mitochondrial dysfunction, yet BHB's role in IIR remains unclear. Using C57BL/6 mouse IIR models and Caco2 cell hypoxia-reoxygenation (HR) models, we identified a pathogenic mechanism: IIR induced nearly 10-fold elevation of intestinal BHB, while ketolytic enzymes 3-hydroxybutyrate dehydrogenase 1 (BDH1) and 3-oxoacid CoA-transferase 1 (OXCT1) were significantly downregulated, blocking BHB's metabolic pathway. Exogenous BHB administration failed to protect the intestine; instead, it selectively inhibited expression of histone deacetylase 2 (HDAC2) (by 30%) and disrupted its nuclear binding to the Sirt7 promoter, promoting Sirt7 gene transcriptional activation (mRNA upregulated by 2-fold). This cascade exacerbated oxidative stress (reactive oxygen species increased by 2.7-fold), reduced adenosine triphosphate levels (by 20%), impaired mitochondrial biogenesis (decreased mitochondrial DNA copy number and mitochondrial transcription factor A (TFAM)/mitochondrial ribosomal proteins (MRPs) expression), and aggravated intestinal barrier dysfunction (Claudin-1 reduced and D-lactate elevated). Notably, HDAC2 overexpression or SIRT7 knockdown reversed these impairments. Our findings uncover a previously unrecognized role of BHB in exacerbating IIR injury via the HDAC2/SIRT7 pathway, providing new insights for protecting pathological intestinal tissues at ischemic risk and targeting mitochondrial biogenesis.

Background CD36, a lipid transporter, is markedly upregulated in the diabetic kidney. However, whether CD36 contributes to renal injury following myocardial ischemia–reperfusion (I/R) in diabetes remains unknown. This study aimed to identify the role of CD36 in myocardial I/R-induced renal injury in diabetic rats and to investigate the mechanisms involved. Methods Type 1 diabetic rats received intravenous SSO, a CD36 inhibitor, and were then subjected to myocardial ischemia-reperfusion (I/R) with ischemic postconditioning. Cardiac and renal function, tissue injury markers, and oxidative stress were assessed using commercial assay kits. Protein expression was analyzed by Western blotting. Results After myocardial I/R, oxidative stress increased and renal function deteriorated. CD36 and the PI3K/Akt/eNOS pathway were upregulated in the kidney, potentially reflecting a compensatory protective response. SSO, a CD36 inhibitor, reduced myocardial injury, lowered renal CD36 and p-Akt/p-eNOS expression, and attenuated renal injury, indicating that its renoprotective effect was largely secondary to cardioprotection. In contrast, ischemic postconditioning conferred little protection in diabetic rats. Conclusions These findings indicate that CD36 is upregulated in the kidney after myocardial I/R in diabetic rats, accompanied by alterations in the PI3K/Akt/eNOS pathway as a compensatory response. CD36 inhibition by SSO reduced myocardial injury and, in turn, attenuated renal injury, suggesting that CD36 is associated with myocardial I/R-induced renal injury.

Hydrogen sulfide (H2S) performs essential functions in several physiological and pathological procedures, such as redox status modulation, anti-inflammation, and so on. It also occurs in wastewater and is associated with food spoilage. In this study, a fluorescent probe NLH was designed and synthesized for the specific recognition of H2S, employing Nile Red as the fluorophore and a cyanate ester group as the recognition unit. The performance of the probe was characterized by excellent stability, a rapid response (30 s), a low detection limit of 0.626 mu M, minimal cytotoxicity, and a wide pH tolerance range (4-9) under physiological conditions. Rapid test strips and swabs fabricated based on probe NLH were capable of both quantifying H2S in water samples across a range of concentrations and dynamically monitoring its production during the spoilage of different foods. Furthermore, probe NLH successfully imaged both exogenous and endogenous H2S in nude mouse models and was effectively applied to models of LPS-induced arthritis and acute liver injury, visually monitoring H2S concentration fluctuations during disease progression, thereby providing a novel molecular tool and visual method for investigating the development as well as monitoring and treatment of these diseases.

Introduction Hypertension constitutes the primary health burden of cardiovascular diseases, and the global control of blood pressure (BP) remains insufficient. Single pill combinations (SPCs) are employed as a means to streamline the management of poor BP control due to non-adherence and treatment inertia. The compound reserpine and triamterene tablets constitute a quadruple SPC, comprising reserpine 0.1 mg, dihydralazine 12.5 mg, hydrochlorothiazide 12.5 mg and triamterene 12.5 mg. It is widely employed in primary medical institutions and has favourable efficacy, tolerability and cost-effectiveness.Methods and analysis The COSPQ-BP trial is a 12-week prospective randomised controlled trial to enrol 1332 patients with primary mild-to-moderate hypertension. Participants who meet the inclusion criteria will be randomly assigned to a 1:1 ratio to an intervention group (compound reserpine and triamterene tablets) or a control group (valsartan/hydrochlorothiazide). The primary outcome will be mean changes from baseline in 24-hour ambulatory systolic BP after intervention for 12 weeks. The secondary outcomes have been predetermined and will primarily encompass the following: (1) changes in other BP measures, as well as changes in blood lipids, blood glucose and uric acid at 12 weeks and (2) evaluation of the impact of starting antihypertensive therapy with compound reserpine and triamterene tablets or valsartan/hydrochlorothiazide on the depressive and anxiety statess of patients.Ethics and dissemination The study protocol (version number: V5.0, version date: 17 January 2023) has been approved by the ethics committee (Biomedical Ethics Committee of West China Hospital of Sichuan University, approval number: Review (51) in 2023). Written informed consent will be obtained from each participant by researchers. The findings of this study will be disseminated through conference presentations and peer-reviewed publications.Trial registration This study was registered at the Chinese Clinical Trials Registry (ChiCTR2300067920). The COSPQ-BP trial is currently enrolling. The study period will be from 1 January 2024 to 31 December 2025.

Sestrin2 is a stress-inducible protein that exhibits protective effects against ischemia-reperfusion injury in various organs. However, the specific roles and mechanisms of Sestrin2 in intestinal ischemia-reperfusion (IIR) injury have yet to be fully elucidated. The present study aims to investigate the role of Sestrin2 in intestinal IIR injury and its underlying mechanisms. We found that in the IIR model of C57BL/6 J mice, Sestrin2 expression increased following IIR injury, accompanied by enhanced lysosomal activity and autophagy activation. Further cellular experiments demonstrated that overexpression of Sestrin2 increased autophagic flux, enhanced lysosomal activity, and mitigated cellular injury. These effects were abrogated by Sestrin2 knockdown. Additionally, we discovered that Sestrin2 interacts with transcription factor EB (TFEB), and that knockdown of Sestrin2 resulted in decreased nuclear translocation of TFEB, leading to a reduction in autophagic flux due to impaired lysosomal function. The TFEB activator (TFEB A1) promoted TFEB nuclear translocation and reversed autophagy/lysosomal pathway (ALP) dysfunction and cellular damage caused by Sestrin2 knockdown. In conclusion, Sestrin2 protects against IIR injury by promoting TFEB nuclear translocation, enhancing lysosomal activity, accelerating autophagosome turnover and substrate degradation, and increasing autophagic flux. These findings provide novel insights and potential targets for the treatment of IIR injury.

Postinduction hypotension (PIH) increases the risk of perioperative adverse events. This study aimed to test if low-dose esketamine could significantly decrease the incidence of PIH in elderly patients undergoing elective noncardiac surgery. This was a post hoc analysis of a randomized clinical trial in university-affiliated academic tertiary hospital. Patients (65 to 85 years, ASA physical status classification II or III) randomly received esketamine (0.2 mg/kg) or normal saline intravenous injection before general anesthesia induction. The primary outcome was the incidence of PIH. The secondary outcomes were the profiles of induction and adverse events during postinduction period. Several different definitions of hypotension and postinduction period were prespecified as the sensitivity analysis. The baseline characteristics were comparable between esketamine group (n = 211) and normal saline group (n = 213). The incidence of PIH was significantly lower in esketamine group than that in normal saline group (44.1 vs. 64.8%, P < 0.01). Esketamine pretreatment significantly decreased the consumption of propofol (P < 0.01) and the rate of vasoconstrictor utilization (P = 0.02). There were no significant differences in the incidence of postinduction adverse events between two groups (all P > 0.05). And, no other severe adverse events were observed. The sensitivity analysis displayed the robustness of the conclusion, though the effect size was lower than 0.2 under certain definition of PIH. A low dose of esketamine treatment before general anesthesia induction for elderly patients undergoing noncardiac surgery could significantly reduce the risk of PIH.Trial registration: www.chictr.org.cn (ChiCTR2100051179); registered 15 September 2021. Date of enrolment of the first participant to the trial: 24 February 2022.

Objective Sodium dithionite (Na2S2O4) is a common reducing agent widely used in the food, textile, biological science, and other fields. Excessive intake of Na2S2O4 can cause stomach cramps, upper respiratory tract infections, and other types of cell-damaging diseases, such as laryngospasm and bronchospasm. Therefore, a rapid, real-time, and in situ detection method for Na2S2O4 is extremely crucial to establish in biological technology, food security supervision, and the environment. Magnetic resonance/fluorescence dual-mode imaging can not only provide high-resolution structural and histological information but also achieve high-sensitivity functional imaging. In this study, a fluorescence/magnetic resonance dual-modality sodium dithionite molecular probe H2 based on cobalt complexes is designed and developed, using Co3+ as the magnetic resonance unit and 7-diethylaminocoumarin-3-carboxylic acid as the fluorescence unit. The probe combines optical imaging with high sensitivity and selectivity and magnetic resonance imaging with strong tissue penetration ability and high spatial resolution, compensating for the deficiencies of single-modal imaging. Methods Probe H2 is synthesized and characterized by nuclear magnetic resonance (NMR) and mass spectrometry. The identification performance of H2 towards Na2S2O4 in an aqueous solution is studied using a UV?vis spectrophotometer and a fluorescence spectrophotometer. All NMR relaxivity measurements and NMR imaging in vivo are performed on a MesoMR23-060H-I Analyst Analyzing & Imaging system (0.5 T, Shanghai Niumag Corp.). Fluorescence imaging data are collected and processed using Amiview Living Image 2.0 software (PerkinElmer, USA). Results and Discussions The capability of probe H2 ensemble for the detection of Na2S2O4 is studied by UV?vis, fluorescence emission spectrum, and magnetic resonance in Tris buffer solution [V(DMSO)& ratio;V(Tris)=9 & ratio;1, pH=7.4]. To evaluate the selectivity of H2 towards Na2S2O4 against other analytes [Figs. 2(b) and 4(a)], no or little effect on the UV?vis and fluorescence spectrum detection of Na2S2O4 is found in the presence of various competitive analytes. The results demonstrate that H2 can be used as a specific probe for Na2S2O4 sensing in aqueous solution. The detection limit is calculated to be 23 mu mol/L based on a 3 sigma/k under the experimental conditions [Fig. 5(a)]. The relaxivity of H2 is gradually enhanced with the increase in the concentrations of Na2S2O4 (0?280 mu mol/L), which indicates the conversion of diamagnetic Co3+ into paramagnetic Co2+ through the redox reaction of Na2S2O4. Additionally, the corresponding T-2-weighted images of H2 show a continuous decrease in spot brightness as the concentration of Na2S2O4 increased [Fig. 7(a)]. The addition of competitive analytes does not noticeably interfere with the responses of the transverse relaxivity (r(2)) [Fig. 7(b)]. The magnetic resonance/fluorescence dual-mode imaging results (Figs.10 and 11) demonstrate that H2 enables the successful detection of Na(2)S(2)O(4)in vivo and may potentially be used in biomedical diagnosis fields in the future. Conclusions In this study, we design and synthesize a magnetic resonance/fluorescence dual-mode molecular probe H2 for Co(III) complexes using 7-diethylaminocoumarin-3-carboxylic acid (L-2) as a ligand. Its structure is characterized by hydrogen nuclear magnetic resonance and high-resolution mass spectrometry. Probe H2 can specifically identify Na2S2O4. After recognition, the fluorescence signal of the H2 solution is quenched, the transverse relaxation signal is enhanced, and the T-2-weighted image becomes darker. The recognition mechanism is verified by high resolution mass spectrometry and cyclic voltammetry. Probe H2 exhibits good light stability, specific selectivity, a suitable pH under physiological conditions and low cytotoxicity. Using 6?8 weeks of nude mice as a model, probe H2 is successfully applied to the visual detection of exogenous Na2S2O4 by magnetic resonance/fluorescence dual-mode imaging in vivo, which has certain application potential in the biomedical field.

Bisphenol S (BPS) has become extensively used in the manufacturing of consumer products. BPS mainly enters the body through food and water, with oral exposure targeting the gastrointestinal tract. However, its safety profile remains contentious and warrants further investigation. In this study, we aimed to assess whether BPS exerts harmful effects on the body in the absence of overt pathological damage. Our results revealed that although BPS did not lead to significant histopathological damage, it induced intestinal barrier dysfunction. Additionally, in vitro investigations utilizing NCM460 cells and human-derived colorectal organoids demonstrated that BPS exposure induced mitochondrial reactive oxygen species (ROS) levels in intestinal endocrine cells (EECs), upregulating the expression of inflammatory mediators TNF-α and CXCL10. Using a DSS-induced colitis mouse model, it was found that BPS exposure exacerbates the progression of intestinal inflammatory diseases. Analysis of single-cell databases demonstrated a significant reduction in the expression of CHGA, a functional protein of enteroendocrine cells (EECs), in patients with inflammatory bowel disease (IBD). The expression of CHGA showed a significant negative correlation with the expression of IL17. Notably, supplementation with 3-Indoleglyoxylic acid effectively mitigates the intestinal damage induced by BPS. These findings highlight the role of mitochondrial oxidative stress and IL-17/CXCL10/TNF-α signaling in BPS-induced intestinal damage and demonstrate the therapeutic potential of 3-Indoleglyoxylic acid in mitigating these effects.

A fluorescence/magnetic resonance (MR) dual-mode molecular probe H1 based on cobalt(III) complexes was designed and synthesized in this work for the detection of sodium dithionite (Na2S2O4) and real-time biological imaging in vivo. The probe combines highly sensitive fluorescence imaging technology and high-resolution magnetic resonance imaging (MRI) technology to address the limitations of each individual modality. Probe H1 used Co3+ as the MRI unit and 3-acetylacetone-7-diethylamino-coumarin as the fluorescence unit. The diamagnetic Co3+ is reduced to paramagnetic Co2+ through the strong reductivity of Na2S2O4, and the MR signal and the fluorescence signal can be activated simultaneously due to the change in magnetic properties of the cobalt ion and the paramagnetic quenching effect of Co2+. Probe H1 demonstrates excellent detection performance in monitoring Na2S2O4, including excellent selectivity, high sensitivity (LOD = 9 μM), and anti-interference. Furthermore, probe H1 was successfully applied to the detection of exogenous Na2S2O4in vivo through magnetic resonance/fluorescence dual-mode imaging, which can potentially be used in the pathological hypoxic microenvironment field in the future.