Wei Xu,Weiping Jin,Chunlan Zhang,Zhenshun Li,Liufeng Lin,Qing Huang,Shuxin Ye,Bin Li
A facile approach to fabricate micro-complex in moderate condition via self-assembly of κ -carrageenan (CRG) and lysozyme (Lys) was investigated for the first time to encapsulate and protect curcumin . The interaction between CRG and Lys, size and morphology were studied by zeta potential, UV–vis spectroscopy, circular dichroism (CD), scanning electron microscope (SEM), transmission electron microscopy (TEM) and X-ray photoelectron spectroscopy (XPS). A tentative interactive model was proposed for polysaccharide and protein. The results indicated that the spherical shaped CRG/Lys complex with 1 μm diameter was spontaneously formed by one spot incubating. Both CRG and Lys were participated in forming the shell of micro-complex synthesized through physical interactions. The encapsulation efficiency (EE) and loading capacity (LC) of curcumin for the CRG/Lys complex prepared with CRG/Lys ratio 2:1 were 71 ± 0.02% and 50.71 ± 0.71 μg ml − 1 respectively. The stability of curcumin loaded in complex was improved about 2.7 fold, 2 fold and 1.7 fold when disposed with 80 °C treatment for 1 min, 60 °C treatment for 30 min and ultraviolet radiation for 2 h. DPPH measurement verified the protection of bioactivity as encapsulated. The worthwhile endeavor elucidated proteins/polysaccharides complex was feasible to solubilize and protect sensitive amphiphilic bioactive compounds and has extensive potential in food and medicinal application with various purposes.
Mitochondrial dysfunction-mediated ribosomal translation suppression is a hallmark of aging and a major driver of degenerative diseases, limiting mRNA therapy efficacy. Here, ionizable coenzyme Q10 (iCoQ10)-engineered lipid/fiber microplexes (iCLNP@SF) are developed that restore the mitochondrial-ribosomal axis to enhance mRNA translation. iCoQ10 replaces conventional ionizable lipids to form prodrugged lipid nanoparticles (iCLNP), stabilized by injectable polydopamine‑modified short fibers for in situ administration. In vitro efficacy assessments showed that iCLNP@SF synergistically enhanced mitochondrial metabolism and mRNA translation in senescent cells. Further mechanistic studies revealed that iCLNP stabilized mitochondrial membrane potential, suppressed cGAS-STING activation, and reduced eIF2α phosphorylation, thereby enhancing translation. In vivo, iCLNP@SF delivery of Gas6 mRNA increased hair follicle density by ≈50% in an androgenetic alopecia mouse model, while Runx2 mRNA delivery raised new bone formation (BV/TV) to ≈40% in defect models, both markedly outperforming conventional LNPs. Together, these findings highlight a strategy that improves mRNA therapy for degenerative diseases.
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