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Lunhao Bai

Researcher at China Medical University (PRC)

Publications -  46
Citations -  649

Lunhao Bai is an academic researcher from China Medical University (PRC). The author has contributed to research in topics: Medicine & Chemistry. The author has an hindex of 10, co-authored 35 publications receiving 305 citations.

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Journal ArticleDOI

P2X7 Receptor Induces Pyroptotic Inflammation and Cartilage Degradation in Osteoarthritis via NF-κB/NLRP3 Crosstalk.

TL;DR: In this paper, the P2X7 receptor was found to activate extracellular matrix degradation and pyroptotic inflammation in OA chondrocytes through NF-κB/NLRP3 crosstalk, thus aggravating the symptoms of OA.
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miR-23a suppresses proliferation of osteosarcoma cells by targeting SATB1.

TL;DR: It is demonstrated that miR-23a is frequently downregulated in osteosarcoma specimens and cell lines compared with adjacent noncancerous tissues and cell line, and its inhibitory effect on tumor are mediated chiefly through downregulation of SATB1.
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The Therapeutic Effects of Treadmill Exercise on Osteoarthritis in Rats by Inhibiting the HDAC3/NF-KappaB Pathway in vivo and in vitro.

TL;DR: It is found that moderate-intensity treadmill exercise could relieve OA and the selective HDAC3 inhibitor RGFP966 could also alleviate inflammation in OA rat model through inhibition of nuclear translocation of NF-kappaB.
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Protectin DX attenuates IL-1β-induced inflammation via the AMPK/NF-κB pathway in chondrocytes and ameliorates osteoarthritis progression in a rat model.

TL;DR: PDX suppresses inflammation in chondrocytes in vitro and in vivo, likely through the AMPK/NF-κB signaling pathway, and the results suggest that PDX could be a useful novel therapeutic agent for OA treatment.
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Mechanical stress protects against osteoarthritis via regulation of the AMPK/NF-κB signaling pathway.

TL;DR: The findings indicate that mechanical stress had no therapeutic effects on normal articular cartilage and chondrocytes; mechanical stress only caused damage with excessive stimulation; Still, moderate biomechanical stress could reduce sensitization to the inflammatory response of articular Cartilage and ChondroCytes through the AMPK/NF‐κB signaling pathway.