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Nana Shi,Kaiyue Sun,Zedi Zhang,Juan Zhao,Lina Geng,Yuhua Lei 한국공업화학회 2021 Journal of Industrial and Engineering Chemistry Vol.101 No.-
Carbon dot (CDs) were prepared for carrying DOX (Doxorubicin) or FAC (Ferric ammonium citrate), andthe loading mechanism and release kinetics of CDs-drugs were studied. CDs were prepared using peonypollen and urea, and characterized by TEM, XRD, 13C NMR, XPS, UV, FT-IR, DLS and zeta potential. Theobtained CDs were rich of –NH2 group on the surface, amorphous phase, spherical morphology withthe diameter about 5 nm, and had a blue fluorescence with the quantum yield (QY) of 12%. Iron disorderscan cause cancer or anemia. DOX is used for treating cancer, but has severe side effects. FAC is an ironsupplement agent, but had low bioavailability. CDs carried DOX (or FAC) through –N=C– (or –CONH–)bond, had high loading efficiency for DOX (37.2%) and FAC (54.0%) by optimizing mass ratios of mCDsto mdrug and reacted overnight. Cellular experiments showed that CDs-drugs had lower cytotoxicity thanfree drugs and CDs co-located with the drug. In vitro release indicated that CDs-DOX had pH-targetedproperty and CDs-FAC could be absorbed easily. CDs-drug release belonged to Weibull model, and releasemechanism was determined by the bonding way between CDs and drug. CDs had potential applicationsin delivery drugs with –C=O or –COOH group.
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Liang Li,Zhang Fengmei,Feng Naibo,Kuang Biao,Fan Mengtian,Chen Cheng,Pan Yiming,Zhou Pengfei,Geng Nana,Li Xingyue,Xian Menglin,Deng Lin,Li Xiaoli,Kuang Liang,Luo Fengtao,Tan Qiaoyan,Xie Yangli,Guo Fen 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-
Osteoarthritis (OA) is a full-joint, multifactorial, degenerative and inflammatory disease that seriously affects the quality of life of patients due to its disabling and pain-causing properties. ER stress has been reported to be closely related to the progression of OA. The inositol-requiring enzyme 1α/X-box-binding protein-1 spliced (IRE1α/XBP1s) pathway, which is highly expressed in the chondrocytes of OA patients, promotes the degradation and refolding of abnormal proteins during ER stress and maintains the stability of the ER environment of chondrocytes, but its function and the underlying mechanisms of how it contributes to the progression of OA remain unclear. This study investigates the role of IRE1α/ERN1 in OA. Specific deficiency of ERN1 in chondrocytes spontaneously resulted in OA-like cartilage destruction and accelerated OA progression in a surgically induced arthritis model. Local delivery of AdERN1 relieved degradation of the cartilage matrix and prevented OA development in an ACLT-mediated model. Mechanistically, progranulin (PGRN), an intracellular chaperone, binds to IRE1α, promoting its phosphorylation and splicing of XBP1u to generate XBP1s. XBP1s protects articular cartilage through TNF-α/ERK1/2 signaling and further maintains collagen homeostasis by regulating type II collagen expression. The chondroprotective effect of IRE1α/ERN1 is dependent on PGRN and XBP1s splicing. ERN1 deficiency accelerated cartilage degeneration in OA by reducing PGRN expression and XBP1s splicing, subsequently decreasing collagen II expression and triggering collagen structural abnormalities and an imbalance in collagen homeostasis. This study provides new insights into OA pathogenesis and the UPR and suggests that IRE1α/ERN1 may serve as a potential target for the treatment of joint degenerative diseases, including OA.
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