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Your search keyword '"Xuan, Jiang‐Wei"' showing total 2 results
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2 results on '"Xuan, Jiang‐Wei"'

1. Downregulating PI3K/Akt/NF-κB signaling with allicin for ameliorating the progression of osteoarthritis: in vitro and vivo studies.

Author

Qian YQ, Feng ZH, Li XB, Hu ZC, Xuan JW, Wang XY, Xu HC, and Chen JX

Subjects
Animals, Bone Density Conservation Agents adverse effects, Bone Density Conservation Agents metabolism, Cell Survival, Cells, Cultured, Chondrocytes cytology, Chondrocytes pathology, Disease Progression, Disulfides, Female, Gene Expression Regulation, Humans, Interleukin-1beta antagonists & inhibitors, Interleukin-1beta genetics, Interleukin-1beta metabolism, Male, Mice, Inbred C57BL, NF-kappa B agonists, NF-kappa B antagonists & inhibitors, NF-kappa B metabolism, Osteoarthritis, Knee metabolism, Osteoarthritis, Knee pathology, Osteoarthritis, Knee physiopathology, Phosphatidylinositol 3-Kinase chemistry, Phosphatidylinositol 3-Kinase metabolism, Proto-Oncogene Proteins c-akt agonists, Proto-Oncogene Proteins c-akt antagonists & inhibitors, Proto-Oncogene Proteins c-akt metabolism, Random Allocation, Recombinant Proteins chemistry, Recombinant Proteins metabolism, Signal Transduction, Sulfinic Acids adverse effects, Sulfinic Acids metabolism, Bone Density Conservation Agents therapeutic use, Chondrocytes metabolism, Dietary Supplements adverse effects, Disease Models, Animal, Osteoarthritis, Knee therapy, Phosphoinositide-3 Kinase Inhibitors, Sulfinic Acids therapeutic use
Abstract

Osteoarthritis (OA) is characterized by the degeneration and destruction of articular cartilage. Allicin, a dietary garlic active constituent, exerts anti-inflammatory effects on several diseases. However, its effects on OA have not been clearly elucidated. In this study, we explored the effects of allicin on OA in both in vitro and in vivo models. Allicin inhibited interleukin-1β (IL-1β) induced overproduction of nitric oxide, inducible nitric oxide synthase, prostaglandin E2, and cyclooxygenase-2, as well as pro-inflammatory cytokines tumor necrosis factor alpha and interleukin-6 in chondrocytes in a dose-dependent manner. Meanwhile, allicin reversed the overproduction of metalloproteinase-13 and a disintegrin and metalloproteinase with thrombospondin motifs-5 and the decrease of aggrecan and type II collagen. Furthermore, allicin dramatically suppressed IL-1β-stimulated PI3K/Akt/NF-κB activation in chondrocytes. In vivo, treatment with allicin prevented the destruction of cartilage and inhibited PI3K/Akt/NF-κB activation in the cartilage of mice OA models. Taken together, these results indicate that allicin may be a potential therapeutic agent for OA.

Published
2018
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2. Hydroxysafflor yellow A (HSYA) targets the NF-κB and MAPK pathways and ameliorates the development of osteoarthritis.

Author

Hu ZC, Xie ZJ, Tang Q, Li XB, Fu X, Feng ZH, Xuan JW, Ni WF, and Wu AM

Subjects
ADAMTS5 Protein genetics, ADAMTS5 Protein metabolism, Animals, Chalcone administration & dosage, Cyclooxygenase 2 genetics, Cyclooxygenase 2 metabolism, Dinoprostone metabolism, Humans, Interleukin-1beta genetics, Interleukin-1beta metabolism, Male, Mice, Mice, Inbred C57BL, NF-kappa B genetics, Nitric Oxide metabolism, Nitric Oxide Synthase Type II genetics, Nitric Oxide Synthase Type II metabolism, Osteoarthritis genetics, Osteoarthritis metabolism, Tumor Necrosis Factor-alpha genetics, Tumor Necrosis Factor-alpha metabolism, Chalcone analogs & derivatives, MAP Kinase Signaling System drug effects, NF-kappa B metabolism, Osteoarthritis prevention & control, Quinones administration & dosage
Abstract

The inflammatory environment has been demonstrated to be strongly associated with the progression of osteoarthritis (OA). HSYA, the main active component in the medical and edible dual purpose plant safflower, has previously showed significant anti-inflammatory effects in several diseases. In the current study, the protective effects of HSYA in the inhibition of OA development and its underlying mechanism were examined by both in vitro and in vivo experiments. Our data indicated that interleukin-1 beta (IL-1β) induced over-production of pro-inflammatory cytokines, such as nitric oxide (NO) and prostaglandin E2 (PGE2); also, the expression of cyclooxygenase-2 (COX-2), tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6) and inducible nitric oxide synthase (iNOS) were all inhibited by pretreatment with HSYA in a dose-dependent manner (2.5 to 40 μM). Furthermore, HSYA attenuated IL-1β-induced degradation of the extracellular matrix (ECM) by decreasing the expression of metalloproteinases (MMPs) and thrombospondin motifs 5 (ADAMTS5). Mechanistically, HSYA suppressed IL-1β-induced activation of the nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) cascades. Meanwhile, molecular docking studies revealed that HSYA has excellent binding abilities to p65, extracellular signal-regulated kinase (ERK), p38 and c-Jun N-terminal kinase (JNK). In addition, the protective effects of HSYA were observed in a surgically induced mouse OA model. In summary, this study provides evidence that HSYA can be applied as a potential therapeutic agent in the treatment of OA.

Published
2018
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