Xiaoliang Xiang

Stanniocalcin-1 (STC-1) is a multifunctional glycoprotein; however, its role in protecting intestinal epithelial cells against oxidative injury has not been completely elucidated. This study investigated the cytoprotective effects and underlying molecular mechanisms of STC-1 overexpression in porcine intestinal epithelial (IPEC-J2) cells subjected to tert-butyl hydroperoxide (TBHP)-induced oxidative stress. IPEC-J2 cells were transfected with pcDNA3.1/STC-1 prior to TBHP challenge. STC-1 overexpression markedly rescued cells from TBHP-induced cytotoxicity and cell death, and was associated with a reduced Bax/Bcl-2 ratio. Concurrently, elevated STC-1 expression dramatically suppressed intracellular reactive oxygen species and mitochondrial superoxide accumulation while preserving the mitochondrial membrane potential. These physiological improvements were accompanied by enhanced total antioxidant capacity and activities of key antioxidant enzymes. Mechanistically, STC-1 overexpression enhanced autophagic flux and promoted Pink1/Parkin-mediated mitophagy to eliminate dysfunctional mitochondria. Furthermore, STC-1 upregulation potentiated the AMPK–Nrf2/Sirt1 signaling axis and the subsequent transcriptional upregulation of mitochondrial quality control markers, including FoxO1, PGC-1α, and TFAM, under stress conditions. Collectively, these findings demonstrate that STC-1 safeguards porcine intestinal cells against oxidative injury by orchestrating a cooperative defense network encompassing ROS scavenging, mitochondrial homeostasis, and antioxidant defense amplification via the AMPK–Nrf2/Sirt1 pathway, highlighting a potential therapeutic target for preventing stress-associated intestinal disorders in piglets.

Stanniocalcin‑1 (STC‑1) is a multifunctional glycoprotein, yet its role in mitigating intestinal epithelial oxidative injury remains elusive. This study investigated the cytoprotective effects and underlying molecular mechanisms of STC‑1 in porcine intestinal epithelial cells (IPEC‑J2) subjected to tert‑butyl hydroperoxide (TBHP)‑induced oxidative stress. IPEC‑J2 cells were transfected with pcDNA3.1/STC‑1 prior to the TBHP challenge. STC‑1 overexpression markedly rescued IPEC‑J2 cells from TBHP‑induced cytotoxicity and apoptosis, as demonstrated by AO/PI dual-staining and a restored Bax/Bcl‑2 ratio. Concurrently, STC‑1 dramatically suppressed intracellular reactive oxygen species and mitochondrial superoxide accumulation while preserving the mitochondrial membrane potential. These physiological improvements were accompanied by enhanced total antioxidant capacity and upregulated activities of key antioxidant enzymes. Mechanistically, mRFP‑GFP‑LC3 reporter assays revealed STC‑1 enhanced autophagic processing and promoted Pink1/Parkin-mediated mitophagy to clear dysfunctional mitochondria. Furthermore, STC‑1 enhanced the AMPK–Nrf2/Sirt1 signaling axis, leading to Keap1 downregulation and the subsequent transcription of mitochondrial biogenesis markers (FoxO1, PGC‑1α, and TFAM) under stress conditions. Taken together, these findings demonstrate that STC‑1 safeguards porcine intestinal epithelial cells against oxidative injury by orchestrating a cooperative defense network that involves ROS scavenging, mitochondrial homeostasis, and antioxidant defense amplification via AMPK–Nrf2/Sirt1 pathway, presenting a potential therapeutic target for preventing stress-associated intestinal disorders in piglets.

Sinomenine, a bioactive alkaloid from Sinomenium acutum, exhibits anti-inflammatory and neuroprotective effects, but its role in neuronal differentiation and morphological maturation remains unclear. This study used Neuro-2a cells and primary neural stem/progenitor cells (NSPCs) to examine the pro-differentiation effects of sinomenine. Sinomenine increased Neuro-2a cell viability at concentrations of 0.1–20 μM and showed no detectable cytotoxicity up to 100 μM. Under differentiation conditions, sinomenine enhanced neuronal differentia-tion and neurite outgrowth in Neuro-2a cells dose-dependently (5–50 μM), increased the proportion of β-tubulin III–positive neurons, promoted multi-neurite formation, and enhanced dendritic comple-xity in NSPCs. Mechanistically, sinomenine selectively induced Akt phosphorylation without activating ERK, p38, or JNK pathways, and pharmacological inhibition of Akt abolished sinomenine-induced neuritogenesis. These findings suggest sinomenine promotes neuronal differentiation and neurite outgrowth via the Akt pathway, supporting its potential in neuroregeneration.

In this study, we introduce a novel hybrid technique for fabricating two-dimensional paper-based microfluidic analytical devices (μPADs) that combines capillary-driven wax patterning with embossing. The method utilizes capillary action to guide molten wax through a sealed polydimethylsiloxane microfluidic chip onto a glass substrate, where it forms high-resolution wax stamps upon demolding. The wax-glass assembly is then heated to facilitate wax penetration through the paper matrix, creating well-defined hydrophobic-hydrophilic barriers. This process allows precise control over stamp dimensions, offering considerable design flexibility. We systematically examined the relationship between flow time and channel length, with experimental results showing strong consistency with a modified Lucas-Washburn model developed in this study. Furthermore, the technique supports seamless integration of biological and chemical sensors into patterned μPADs, enabling the fabrication of fully functional devices. Our results highlight the robustness and scalability of this combined approach, achieving a remarkably reduction of cost. Combined with its operational simplicity, this method is particularly suitable for large-scale applications in resource-limited environments.

This study proposes a simple yet versatile microfluidic strategy for fabricating monodisperse alginate hydrogel microspheres using a symmetric flow-focusing device. The system integrates three key innovations: (1) Cost-effective mold fabrication: A paper-based positive master replaces conventional SU-8 photoresist, significantly simplifying device prototyping. (2) Surfactant-free droplet generation: Alginate hydrogel droplets are formed at the first flow-focusing junction without requiring interfacial stabilizers. (3) In situ solidification with coalescence suppression: Acetic acid-infused corn oil is introduced at the adjacent junction, simultaneously triggering ionic crosslinking of alginate via pH reduction while preventing droplet aggregation. Notably, the hydrogel microspheres can be efficiently harvested through oscillatory aqueous phase separation, removing post-fabrication washing steps (typically 6–8 cycles for surfactant and oil removal). This integrated approach demonstrates exceptional advantages in fabrication simplicity, process scalability, and operational robustness for high-throughput hydrogel microsphere production.

This study proposes a simple yet versatile microfluidic strategy for fabricating monodisperse alginate hydrogel microspheres using a symmetric flow-focusing device. The system integrates three key innovations: (1) Cost-effective mold fabrication: A paper-based positive master replaces conventional SU-8 photoresist, significantly simplifying device prototyping; (2) Surfactant-free droplet generation: Alginate hydrogel droplets are formed at the first flow-focusing junction without requiring interfacial stabilizers; (3) In situ solidification with coalescence suppression: Acetic acid-infused corn oil is introduced at the adjacent junction, simultaneously triggering ionic crosslinking of alginate via pH reduction while preventing droplet aggregation. Notably, the hydrogel microspheres can be efficiently harvested through oscillatory aqueous phase separation, removing post-fabrication washing steps (typically 6-8 cycles for surfactant and oil removal). This integrated approach demonstrates exceptional advantages in fabrication simplicity, process scalability, and operational robustness for high-throughput hydrogel microsphere production.

Galanthamine, an alkaloid from the Amaryllidaceae family, serves as an inhibitor of acetylcholinesterase. Beause of its central cholinergic properties, galanthamine is currently being researched as a potential therapeutic agent for the treatment of Alzheimer's disease. Nevertheless, the full extent of its other biological activities is still unclear. Here, we investigated the therapeutic potential of galanthamine in inducing neuronal differentiation and enhancing neurite outgrowth in neural stem and progenitor cells (NSPCs). Our comprehensive analysis revealed significant alterations in neuronal morphology and complexity during neuronal maturation following galanthamine treatment. Specifically, galanthamine significantly increased the percentage of multiple-neurite neurons, suggesting its ability to stimulate neurite formation and promote the development of extensive neuronal networks. Additionally, treatment with galanthamine resulted in a considerable increase in the proportion of mature-appearing neurons, characterized by elongated and intricate dendrites, suggesting its potential in enhancing neural plasticity and repair. Importantly, we further confirmed that galanthamine promotes neuronal differentiation in NSPCs through up-regulation of the IGF2 signaling pathway. Altogether, these findings contribute significantly to our understanding of the effects of galanthamine on Alzheimer's disease and underscore its potential as a therapeutic agent for this neurodegenerative condition.

Galanthamine, an alkaloid derived from the Amaryllidaceae family, serves as an acetylcholinesterase inhibitor. Due to its central cholinergic properties, this compound is being actively studied as a potential treatment for Alzheimer’s disease. However, the broader scope of its biological effects remains poorly understood. In this study, we explored the therapeutic potential of galanthamine in promoting neuronal differentiation and enhancing neurite outgrowth in neural stem and progenitor cells (NSPCs). Our detailed analysis demonstrated notable changes in neuronal morphology and complexity during maturation following galanthamine exposure. Notably, the compound significantly increased the proportion of neurons with multiple neurites, indicating its ability to stimulate neurite formation and foster the development of complex neuronal networks. Furthermore, galanthamine treatment led to a marked rise in the number of mature-appearing neurons, distinguished by elongated and intricate dendrites, highlighting its potential to enhance neural plasticity and repair mechanisms. Importantly, we also identified that galanthamine facilitates neuronal differentiation in NSPCs by up-regulating the insulin-like growth factor 2 signaling pathway. Collectively, these findings provide valuable insights into galanthamine’s role in Alzheimer’s disease and emphasize its promise as a therapeutic agent for this neurodegenerative disorder.

Adult neurogenesis involves the generation of functional neurons from neural progenitor cells, which have the potential to complement and restore damaged neurons and neural circuits. Therefore, the development of drugs that stimulate neurogenesis represents a promising strategy in stem cell therapy and neural regeneration, greatly facilitating the reconstruction of neural circuits in cases of neurodegeneration and brain injury. Our study reveals that compound A5, previously designed and synthesized by our team, exhibits remarkable neuritogenic activities, effectively inducing neurogenesis in neural stem/progenitor cells (NSPCs). Subsequently, transcriptome analysis using high-throughput Illumina RNA-seq technology was performed to further elucidate the underlying molecular mechanisms by which Compound A5 promotes neurogenesis. Notably, comparative transcriptome analysis showed that the up-regulated genes were mainly associated with neurogenesis, and the down-regulated genes were mainly concerned with cell cycle progression. Furthermore, we confirmed that Compound A5 significantly affected the expression of transcription factors related to neurogenesis and cell cycle regulatory proteins. Collectively, these findings identify a new compound with neurogenic activity and may provide insights into drug discovery for neural repair and regeneration.