Baicalin prevents the apoptosis of endplate chondrocytes by inhibiting the oxidative stress induced by H2O2

Abstract

Osteoarthritis (OA) is a degenerative disease of articular cartilage. The pathogenesis of OA remains to be fully elucidated, and several studies have found that oxidative stress is important in its pathogenesis. Baicalin is well known and has already been investigated for its role of inhibiting the oxidative stress pathway. Thus, the present study aimed to investigate the role of baicalin on the inhibition of oxidative stress in endplate chondrocytes induced by hydrogen peroxide (H2O2). Following treatment of endplate chondrocytes with different doses of H2O2 with or without baicalin for different incubation durations, a CCK‑8 assay and Annexin V/PI staining were used to measure the cell proliferation and apoptotic rates to identify the optimal experimental conditions. Subsequently, for examining the effects and underlying mechanism of baicalin on oxidative stress, the protein expression levels of cleaved‑poly (ADP‑ribose) polymerase (PARP), B‑cell lymphoma‑2‑associated X protein (Bax) and pro‑caspase‑3 were analyzed using western blot analysis, intracellular anti‑oxidant activities, including those of malondialdehyde (MDA), superoxide dismutase (SOD) and nitric oxide (NO), were quantified, and the levels of endothelial nitric oxide synthase (eNOS) were examined using reverse transcription‑polymerase chain reaction analysis. The results revealed that the oxidative stress of endplate chondrocytes induced by 0.5 mM H2O2 for 4 h were the most appropriate conditions for experiments, and pretreatment with 100 µmol/l baicalin for 1 h effectively reversed the effect of H2O2 on the endplate chondrocytes. In addition, Annexin V/PI staining demonstrated that the cell death induced by H2O2 was apoptotic, and baicalin reversed the apoptosis induced by oxidative stress. H2O2 activated PARP cleavage, and the expression of Bax and pro‑caspase‑3; however, baicalin inhibited the expression of these apoptotic signaling indicators. Baicalin also reduced the levels of MDA, and increased the levels of SOD and NO. Baicalin also significantly elevated the mRNA levels of eNOS in endplate chondrocytes. Therefore, the results of the present study showed that baicalin significantly inhibited the oxidative stress in endplate chondrocytes induced by H2O2, and decreased cell apoptosis.

<p>Baicalin Protects Human OA Chondrocytes Against IL-1β-Induced Apoptosis and ECM Degradation by Activating Autophagy via MiR-766-3p/AIFM1 Axis</p>

“… 27 Moreover, several literatures demonstrated that baicalin also played a role in ameliorating OA progression. 28 , 29 …”

Hyaluronic Acid Loaded with Cerium Oxide Nanoparticles as Antioxidant in Hydrogen Peroxide Induced Chondrocytes Injury: An In Vitro Osteoarthritis Model

“…Osteoarthritis (OA) is a degenerative disease of articular cartilage induced by various factors. Although OA’s pathogenesis remains to be fully elucidated, it has been generally recognized that overexpression of reactive oxygen species (ROS) plays a vital role in the degeneration of articular cartilage [ 26 ]. Submillimolar concentrations of H 2 O 2 can induce inhibition of the extracellular matrix (ECM) synthesis, chondrocyte apoptosis, lipid peroxidation, and inflammatory cytokines overproduction, and lead to the matrix metalloproteinase (MMPs) formation [ 5 , 6 , 7 ].…”

“…H 2 O 2 -mediated oxidative stress can enhance ROS and lipid peroxidation levels in chondrocytes. Previous studies have shown that chondrocyte apoptosis induced by oxidative stress was responsible for the development of OA [ 26 , 30 , 31 ]; lipid peroxidation could be induced by ROS and caused significant tissue damage in degenerative osteoarthritis [ 32 , 33 , 34 , 35 ].…”

Baicalin promotes extracellular matrix synthesis in chondrocytes via the activation of hypoxia‑inducible factor‑1&alpha;

“…Xing et al (23) concluded that BA protects chondrocytes by inhibiting NF-κB signaling pathways (23). Moreover, it was reported that BA significantly inhibited the oxidative stress and decreased cell apoptosis (25). The HIF-1α pathway generally involves chondrogenesis and cartilage formation of chondrocytes (16).…”