Abstract
The present study aimed to investigate the anti-inflammatory effects of Baicalein on human osteoarthritic chondrocytes and its molecular mechanisms, and to explore the related molecular events that may occur. The extracted human osteoarthritic chondrocytes were stimulated with interleukins. After administered with different concentrations of Baicalein, the survival rate of chondrocytes was observed. Apoptosis was detected by apoptosis assay kit. The effect on NO production was detected using the Griess reagent kit. The expressions of IL-6 and PGE2 were detected by ELISA. The apoptotic proteins and PI3/Akt, NF-kB and MAPK cascade proteins were detected by WB assay. Baicalein significantly increased the survival rate of chondrocytes and decreased the expressions of NO, IL-6 and PGE2. The expressions of COX-2 and induced iNOS were significantly reduced in a dose-dependent manner under the administration of Baicalein. In addition, Baicalein significantly reduced the NF-κB signaling pathway, inhibited the activation of the induced PI3/Akt, JNK, ERK and p38 MAPK cascades. Inflammatory mediators play a key role in the pathogenesis of osteoarthritis. Baicalin significantly inhibits the expression of inflammatory mediators in chondrocytes of human osteoarthritis and regulates the JNK/ERK/p38 MAPK and PBK/Akt signaling cascades. The experiment evaluated the anti-inflammatory and anti-osteomyelitis effects of Baicalein in order to discover new treatment strategies.
Highlights
Osteoarthritis is a degenerative disease of the joint characterized by progressive damage and erosion of the articular cartilage, destruction of the articular surface, exposure of the subchondral bone, and long-term wear and tear, secondary bone hyperplasia, formation of callus and cartilage lower bone sclerosis, joint deformity, chronic pain, limited mobility, and reduced quality of life, which will eventually lead to long-term illness and disability (Riddle & Stratford, 2014; Kato et al, 2014)
The chondrocytes treated with different concentrations of Baicalein were tested by MTT assay to detect whether the drug has cytotoxic effect
After IL-lβ stimulation, it can be seen that Baicalein improved the survival rate of chondrocytes, as shown in Figure 2. 3.2 Baicalein inhibited the production of nitric oxide (NO) and prostaglandin E2 (PGE2) induced by IL-1β stimulation
Summary
Osteoarthritis is a degenerative disease of the joint characterized by progressive damage and erosion of the articular cartilage, destruction of the articular surface, exposure of the subchondral bone, and long-term wear and tear, secondary bone hyperplasia, formation of callus and cartilage lower bone sclerosis, joint deformity, chronic pain, limited mobility, and reduced quality of life, which will eventually lead to long-term illness and disability (Riddle & Stratford, 2014; Kato et al, 2014). Articular chondrocytes maintain a dynamic balance between the synthesis and degradation of extracellular matrix (ECM) components, including n-type collagen and proteoglycans in articular cartilage, the most abundant proteoglycan (PG) (Wojdasiewicz et al, 2014; Yang et al, 2014). Due to the excessive production of inflammatory cytokines and matrix degrading enzymes, the chondrocyte metabolism is imbalanced, and synergistic with the decrease of anabolic signals, eventually leading to the destruction of extracellular matrix and consequent cartilage degeneration. Reactive oxygen species (ROS)-induced oxidative stress further disrupts cartilage homeostasis and promotes catabolism through inducing apoptosis and matrix component destruction, up-regulating potential matrix degrading enzymes, and inhibiting matrix synthesis as well as intracellular and cellular oxidation of external molecules (Tuli et al, 2020). There are pre-clinical reports about the protective effects of Baicalein on bone, such as bone healing, but there are few reports of the drug effect on osteoarthritis, so this direction has a certain degree of innovation (Richette et al, 2010)
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