Retracted Article: Salvianolic acid B inhibits inflammatory response and cell apoptosis<i>via</i>the PI3K/Akt signaling pathway in IL-1β-induced osteoarthritis chondrocytes

Zhu, Bin; Wang, Xuejian

doi:10.1039/c8ra02418a

Cited by 9 publications

(3 citation statements)

References 48 publications

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“…The cartilage tissue pieces were digested with Dulbecco's modified Eagle's medium (DMEM; Gibco) containing 0.2% collagenase and 5% foetal bovine serum (FBS; Invitrogen) overnight following with trypsin at 37°C for 10 minutes . After digestion, the cells were centrifuged at 800 r/min twice for 20 minutes and cultured in DMEM medium supplemented with 10% foetal bovine serum, 100 U/mL penicillin and 100 μg/mL streptomycin.…”

Section: Methodsmentioning

confidence: 99%

Vitexin alleviates interleukin‐1β‐induced inflammatory responses in chondrocytes from osteoarthritis patients: Involvement of HIF‐1α pathway

et al. 2019

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It has been reported that vitexin has anti‐inflammatory effects in osteoarthritis (OA) rats. However, the effects of vitexin on interleukins‐1β (IL‐1β)‐stimulated OA patient‐derived chondrocytes have not been reported. The purpose of this study was to investigate the anti‐inflammatory effects of vitexin on IL‐1β‐stimulated human osteoarthritis chondrocytes and to reveal the involvement of hypoxia‐inducible factor 1α (HIF‐1α) pathway. Enzyme‐linked immunosorbent assay, quantitative real‐time PCR and Western blotting assays were employed. ELISA results demonstrated that the proinflammatory cytokine levels of interleukins‐6 (IL‐6) and tumour necrosis factor α (TNF‐α) in the serum and synovial fluid and HIF‐1α level in the synovial fluid were significantly elevated in OA patients compared to normal healthy subjects. Moreover, the Western blotting results indicated that the protein expression of HIF‐1α was significantly higher in the cartilage tissues of OA patients. OA patient‐derived chondrocytes were stimulated by IL‐1β and treated with different concentration of vitexin for 24 hours. Vitexin showed no cytotoxicity and increased the survival of chondrocytes under IL‐1β stimulation. Vitexin suppressed IL‐1β‐induced production of NO and prostaglandin E2 (PGE2) in chondrocytes culture. The treatment of vitexin significantly inhibited IL‐1β‐induced expressions of proinflammatory cytokine levels of IL‐6, TNF‐α, matrix metalloproteinase (MMP)‐1, MMP‐3 and MMP‐13. Furthermore, Western blotting results demonstrated that HIF‐1α is involved in vitexin's protective effects on IL‐1β‐stimulated injuries in OA patient‐derived chondrocytes. Our study demonstrates that vitexin alleviates IL‐1β‐induced inflammatory responses in chondrocytes from osteoarthritis patients, which may be attributed partly to the inhibition of HIF‐1α pathway.

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Section: Methodsmentioning

confidence: 99%

Vitexin alleviates interleukin‐1β‐induced inflammatory responses in chondrocytes from osteoarthritis patients: Involvement of HIF‐1α pathway

et al. 2019

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“…These results align with those of Zhu et al, where SAB was reported to suppress iNOS expression, thereby mitigating inflammation and cell apoptosis in cartilage cells. 19 These findings suggest that SAB serves as an effective anti-inflammatory and antioxidant agent, preventing oxidative stress and cellular apoptosis.…”

Section: Discussionmentioning

confidence: 94%

Salvianolic Acid B Reduces Oxidative Stress to Promote Hair-Growth in Mice, Human Hair Follicles and Dermal Papilla Cells

Thianthanyakij,

Zhou,

et al. 2024

CCID

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Background: Existing research links oxidative stress and inflammation to hair loss. Salvianolic acid B (SAB) is known for its antioxidative, anti-inflammatory, and other beneficial pharmacological properties. Objective: To assess the efficacy of SAB in modulating hair growth. Methods: In vivo experiments were conducted using C57BL/6 mice to evaluate the effects of SAB on hair and skin parameters. The study involved ex vivo analysis of human hair follicles (HFs) for hair shaft length and hair growth cycle assessment. In vitro, human dermal papilla cells (hDPCs) were cultured with SAB, and their proliferation, protection against H2O2-induced oxidative damage, and gene/protein expression alterations were examined using various analytical techniques, including Real-Time Cell Analysis (RTCA), DCFH-DA Assay, RNA-seq, and KEGG pathway analysis. Results: SAB treatment in mice significantly improved hair growth and vascularization by day 21. In human HFs, SAB extended hair shaft length and delayed the transition to the catagen phase. SAB-treated hDPCs showed a notable decrease in the expression of oxidation-antioxidation-related genes and proteins, including reduced phosphorylation levels of ERK and p38. Conclusion:The study indicates that SAB promotes hDPC proliferation and offers protection against oxidative stress, highlighting its potential as a therapeutic agent for enhancing hair growth and treating hair loss.

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“…It is demonstrated that the inhibition of the P13K/AKT signaling pathway contributes to the mechanisms termed apoptosis and autophagy of chondrocytes [ 42 , 43 ]. After the activation of PI3K, inositol can be phosphorylated, which promotes the activation of AKT directly or indirectly Phosphorylated-AKT is the main form of the activation of AKT [ 44 ]. P-AKT can inhibit apoptosis by suppressing the activity of FKHR, NF-kappa B and GSK-3, inhibiting phosphorylation of Bad, caspase-9 and inhibiting the release of apoptosis factors by mitochondrial [ 45 ]; it can also stimulate the TOR/P70S6‐kinase pathway to suppress the autophagy in mammalian cells [ 46 ].…”

Section: Discussionmentioning

confidence: 99%

Swimming prevents cell death of chondrocytes via PI3K/AKT pathway in an experimental model

Qian

Zhao

et al. 2023

J Orthop Surg Res

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Background Knee Osteoarthritis (KOA) is one of the main causes of disability in the elderly and with limited treatment options. Swimming was considered as an ideal form of non-surgical management of KOA. Nevertheless, the mechanism of swimming intervene OA remains unclear. ACLT induced OA model was often used to study the pathogenesis and treatment of OA. Thus, we evaluated the protective effect of swimming on KOA mouse and tried to explore the underlying mechanism. Methods Forty C57BL/6 mice were randomly divided into five groups: Blank group, ACLT group, ACLT + Swim group, Sham group and Sham + Swim group (n = 8). OA model was established by Anterior Cruciate Ligament Transection surgery (ACLT). After modeling, mice in ACLT + Swim and Sham + Swim groups were trained with a moderate swimming program, 5 d/week, for 6 weeks. HE and Safranin-O/fast staining, Immunohistochemistry, TUNEL assay and Western blot were used to detect the effect of swimming on pathological changes, cell death and the mechanism in KOA mouse. Results Swimming significantly enhanced CoII expression and suppressed ADAMTS5 expression in cartilage of KOA mouse, thus ameliorated KOA development. Apoptotic and autophagic processes were enhanced in OA cartilage, which might be caused by down-regulation of PI3K/AKT pathway; swimming could activate PI3K/AKT pathway and thus regulate apoptosis and autophagy processes of chondrocytes. Conclusion Swimming could prevent cell death of chondrocytes via PI3K/AKT pathways, thus delayed the progression of KOA in an experimental model.

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Retracted Article: Salvianolic acid B inhibits inflammatory response and cell apoptosisviathe PI3K/Akt signaling pathway in IL-1β-induced osteoarthritis chondrocytes

Abstract: Osteoarthritis (OA) is the most common joint disease among late middle-aged or elderly people.

Cited by 9 publications

References 48 publications

Vitexin alleviates interleukin‐1β‐induced inflammatory responses in chondrocytes from osteoarthritis patients: Involvement of HIF‐1α pathway

Vitexin alleviates interleukin‐1β‐induced inflammatory responses in chondrocytes from osteoarthritis patients: Involvement of HIF‐1α pathway

Salvianolic Acid B Reduces Oxidative Stress to Promote Hair-Growth in Mice, Human Hair Follicles and Dermal Papilla Cells

Swimming prevents cell death of chondrocytes via PI3K/AKT pathway in an experimental model

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