Hui Kong

Background: Hyperlipidemia (HL) is a lipid metabolism disorder that contributes significantly to the global burden of metabolic diseases. Hence, novel pharmacological interventions are urgently needed. Our study explored the potential mechanisms by which Crataegi Fructus Carbonisata carbon dots (CFC-CDs) act against hyperlipidemia through in vivo and in vitro experiments. Methods: We prepared CFC-CDs and comprehensively characterized them. Subsequently, we assessed the effects of CFC-CDs on serum lipid profiles in a high-fat diet-induced rat model and used transcriptomic analysis to explore the potential mechanisms underlying their lipid-lowering effects. Additionally, we developed an in vitro model of sodium oleate (OA)-induced lipid deposition in HepG2 cells and validated it using the PPARα inhibitor GW6471. Results: The CFC-CDs had an ultrasmall size ranging from 1.34 to 4.67 nm and an interplanar spacing of approximately 0.210 nm. Their surfaces contained functional groups, including–OH, C=O, and C=N. These CDs exhibited excellent biocompatibility. Animal studies demonstrated that oral treatment with CFC-CDs markedly reduced high-fat diet (HFD)-induced hyperlipidemia. Liver transcriptome analysis indicated that CFC-CDs exerted lipid-lowering effects primarily by activating the PPARα signaling pathway, suggesting that CFC-CDs have significant metabolic reprogramming capabilities. CFC-CDs also exhibited excellent lipid-lowering effects in vitro , and the PPARα inhibitor GW6471 reversed the protective effects of CFC-CDs, thereby leading to lipid accumulation. CFC-CDs may be a potential therapeutic agent for HL. Conclusion: The above evidence suggests that CFC-CDs synthesized by one-step calcination can significantly improve lipid metabolism disorders. Our study shows that CFC-CDs are a biomass-derived carbonaceous nanomaterial exhibiting effective lipid-lowering properties and broadening their potential clinical applications. This research provides crucial insights into the use of CFC-CDs in metabolic disease treatment and lays a solid experimental foundation for developing a new lipid-lowering candidate.

Cost-effective and durable non-noble-metal electrocatalysts are highly desirable for efficient alkaline oxygen evolution reaction (OER). In this study, FeCoNiMn medium-entropy alloy electrocatalysts were prepared on copper substrates by one-step potentiostatic electrodeposition in a choline chloride–urea deep eutectic solvent. By optimizing the deposition potential and MnCl2 concentration, the electrode prepared at −1.6 V with 0.2 M MnCl2 exhibited a hierarchical cauliflower-like particle/nanosheet morphology, which enlarged the electrochemically active surface area and improved surface wettability. The optimized FeCoNiMn electrode delivered an overpotential of 260 mV at 10 mA cm⁻2, a Tafel slope of 103.96 mV dec⁻1, and a charge-transfer resistance of 1.643 Ω cm2, outperforming FeCoNi and commercial RuO2–IrO2 electrodes. Moreover, it showed good stability during long-term chronopotentiometry, multistep current testing, and 2000 CV cycles. Post-OER XPS analysis revealed surface reconstruction with enriched high-valence metal species and oxygen-containing active sites. This work provides a facile electrodeposition strategy for developing efficient medium-entropy alloy electrocatalysts for alkaline OER.

This study concurrently addressed the separation method for carbon dots derived from Glycyrrhizae Radix et Rhizoma Praeparata cum Melle (GRRPM) and the in vitro evaluation of their anti-allergic biological activity. Glycyrrhizae Radix et Rhizoma Praeparata cum Melle Carbon Dots (GRRPM-CDs) were prepared via decoction followed by dialysis, and their properties were characterized using High-Performance Liquid Chromatography (HPLC) and nanomaterial techniques. Anti-allergic activity was evaluated using a C48/80-induced RBL-2H3 mast cell degranulation model. Safety and efficacy were assessed using the CCK-8 assay, direct intervention, and drug-containing serum methods. The release of β-hexosaminidase (β-hex), histamine (HIS), interleukin-4 (IL-4), and tumor necrosis factor-α (TNF-α) was measured by ELISA, and key proteins in the MAPK signaling pathway were analyzed by Western blot. GRRPM-CDs inhibited mast cell degranulation and the release of allergic and inflammatory mediators in a dose-dependent manner. They also significantly downregulated the phosphorylation levels of the JNK, ERK, and p38 proteins in the MAPK signaling pathway. GRRPM-CDs exhibit significant anti-allergic activity, likely via suppression of the MAPK pathway. These findings provide new insights into the bioactive components of processed Glycyrrhiza and suggest potential avenues for developing novel therapies for allergic diseases.

Background: Psoriasis is a chronic, debilitating inflammatory skin disorder mediated by the immune system. It is characterized by excessive keratinocyte proliferation and abnormal differentiation, leading to symptoms that significantly impair the quality of life of affected individuals. Despite extensive research, no effective drugs are currently available to completely inhibit the progression of psoriasis. Purpose: This study aims to explore the therapeutic potential and underlying mechanisms of Phellodendron chinense charcoal carbon dots (PCC-CDs) in treating psoriasis. PCC-CDs have recently garnered attention due to their sustained anti-inflammatory properties and unique bioavailability. Methods: This study explores the therapeutic potential and underlying mechanisms of PCC-CDs in psoriasis treatment via detailed pharmacological experiments in an imiquimod (IMQ)-induced mouse model, including topical PCC-CDs application, inflammatory mediator detection, histopathological assessment of tissue damage, and transcriptomic as well as molecular biology analyses focusing on the modulation of the HMGB1/TLR4 and MAPK/NF-κB inflammatory signaling pathways. Results: In the IMQ-induced mouse model, PCC-CDs effectively suppressed the levels of inflammatory mediators and reduced histopathological damage. Molecular analyses revealed that PCC-CDs may exert their therapeutic effects by modulating the inflammatory response mediated by the HMGB1/TLR4 pathway, primarily through inhibiting protein expression in the MAPK/NF-κB signaling cascade. The application of PCC-CDs resulted in a significant reduction in psoriasis-like symptoms in IMQ-induced mice, including marked improvements in erythema, scaling, and pruritus. Conclusion: PCC-CDs offer a promising new approach to the clinical management of psoriasis. Their ability to provide sustained anti-inflammatory effects and distinctive bioavailability makes them a potential candidate for further development as a therapeutic agent. This study highlights the importance of PCC-CDs in modulating key inflammatory pathways, offering hope for improved treatment options for individuals suffering from psoriasis.

Background: Epilepsy remains a prevalent neurological disorder characterized by spontaneous, recurrent seizures. Despite available treatments, there is a critical lack of safe and effective strategies for long-term management and control. Crinis Carbonisatus (CrCi), the carbonized product of human hair, has been utilized for millennia to manage epilepsy and hemorrhagic disorders in Traditional Chinese Medicine. In our previous work, we successfully isolated Carbon Dots (CrCi-CDs) from CrCi and demonstrated their neuroprotective activity against ischemic stroke. Extending this rationale to seizure management, the present study investigates the potential antiepileptic efficacy of CrCi-CDs in acute epilepsy models. Methods: CrCi-CDs were synthesized via the calcination of human hair at 350 °C, followed by aqueous extraction and purification. To evaluate their antiepileptic potential, acute epilepsy models were established in mice using three distinct chemoconvulsants: Pentylenetetrazole (PTZ), Pilocarpine (PILO), and Penicillin (PNC). We systematically assessed the ability of CrCi-CDs to attenuate seizure severity by modulating neuronal excitability, suppressing neuroinflammation, and mitigating oxidative stress. Furthermore, the PTZ-induced model was specifically selected as a representative paradigm to elucidate the underlying molecular mechanisms. Results and conclusion: This study successfully synthesized spherical CrCi-CDs rich in surface functional groups (hydroxyl, amino, and carboxyl groups), which exhibited excellent dispersibility in aqueous solutions. In vivo evaluations using PTZ, PILO, and PNC models demonstrated that CrCi-CDs significantly reduced the severity of epileptic seizures and attenuated seizure-induced spatial learning and memory deficits. Brain histopathology revealed that CrCi-CDs treatment effectively mitigated hippocampal neuronal damage. Mechanistically, CrCi-CDs exerted neuroprotective effects through multiple pathways: restoring homeostasis by correcting pathological imbalances of neurotransmitters (Glu/GABA), alleviating oxidative stress (SOD/MDA), and suppressing proinflammatory cytokine release (TNF-α, IL-1β, IL-6, IL-18). Further investigations suggest these effects may be mediated by regulating glutamate transporters, inhibiting the NF-κB inflammatory cascade, and modulating neuronal apoptosis pathways. This study confirms that bio-derived CrCi-CDs exhibit potent antiepileptic and neuroprotective properties. By simultaneously targeting neurotransmission, inflammation, and oxidative stress, CrCi-CDs emerge as a highly promising therapeutic candidate with a favorable safety profile, providing a scientific rationale for the development of biomass-derived nanomedicines in epilepsy management.

The Acronicta major larva is a toxic agricultural pest that poses severe ecological management challenges. This study presents a sustainable strategy to valorize this hazardous biological waste into functional nanotherapeutics for insomnia by leveraging its unique intrinsic chemical composition. Carbon dots derived from Acronicta major larva (AM-CDs) were synthesized via one-step pyrolysis, which facilitated the natural molecular pre-assembly of N,S-codoping. Their physicochemical properties and cytotoxicity were evaluated using a series of characterizations and the CCK-8 assay. The sedative and hypnotic effects were assessed in mice with PCPA-induced insomnia through hot plate, Open Field and pentobarbital-induced sleep tests, and their potential mechanism was explored via neurotransmitter detection. The thermal process effectively eliminated intrinsic toxicity while retaining bioactivity via in situ heteroatom doping. AM-CDs exhibited favorable biocompatibility and significant sedative–hypnotic activity, reducing anxiety-related agitation without motor impairment. Mechanistically, AM-CDs effectively restored the GABA/5-HT/glutamate axis. Unlike direct central receptor binding, our findings suggest that this therapeutic effect is likely mediated through a systemic or peripheral regulatory pathway. This study demonstrates the conversion of toxic pests into safe and intrinsically bioactive nanomaterials, providing a dual solution for ecological pest management and novel neuroactive agent development, and validating the “Waste-to-Wealth” concept in biomedicine.

Background: Temporal lobe epilepsy (TLE), a prevalent refractory focal epilepsy frequently complicated by comorbid anxiety and depression, poses significant therapeutic challenges due to the inadequate efficacy of current antiepileptic drugs in seizure control. Carbon dots (CDs) demonstrate notable biological activities and represent a promising class of nanomedicines for TLE intervention. Methods: This study established an eco-friendly calcination protocol to synthesize a novel suspension of Crinis Carbonisatus-derived carbon dots (CC-CDs) as a candidate therapeutic for TLE. Results: In a TLE mouse model, the CC-CDs suspension significantly inhibited phosphorylation of the MAPK pathway (p-JNK, p-ERK, p-p38; p < 0.01, p < 0.05), leading to reduced levels of pro-inflammatory cytokines (IL-6, IL-1β, TNF-α; p < 0.01, p < 0.05), upregulation of TGF-β1 (p < 0.01, p < 0.05), and restoration of antioxidant enzyme activities (SOD, GSH, CAT; p < 0.01, p < 0.05). These modifications subsequently regulated the Glu/GABA balance, alleviating excitotoxicity (p < 0.05), attenuating neuronal damage and Nissl body loss in hippocampal CA1/CA3 regions, and improving cognitive function alongside reducing anxiety-like behaviors (p < 0.01, p < 0.05). In vitro, the CC-CDs suspension suppressed LPS-induced apoptosis in BV2 cells. Conclusions: The CC-CDs suspension ameliorates TLE by inhibiting MAPK signaling, thereby reducing neuroinflammation and oxidative stress, rectifying Glu/GABA imbalance, attenuating excitotoxicity, and ultimately improving behavioral deficits. These findings underscore the therapeutic potential of CC-CDs suspension for TLE treatment.