Casticin protects against IL-1β-induced inflammation in human osteoarthritis chondrocytes

Mu, Yiping; Wu, Hao; Li, Songbai

doi:10.1016/j.ejphar.2018.10.051

Cited by 25 publications

(22 citation statements)

References 32 publications

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“…The effect of tricetin on MMP-1, MMP-3, and MMP-13 mRNA expression was assessed using RT-PCR (Figure 3(a)). The results showed that IL-1 β (10 ng/ml) significantly increased the expression of all three enzymes compared to the untreated control group, in accordance with the previous report [19]. The anticatabolic effect of tricetin at different concentrations was evidenced by its reduction of IL-1 β -induced MMP expression.…”

Section: Resultssupporting

confidence: 90%

Tricetin Protects Rat Chondrocytes against IL-1β-Induced Inflammation and Apoptosis

Sun

Xiong

et al. 2019

Oxidative Medicine and Cellular Longevity

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Tricetin is a well-studied flavonoid with a wide range of pharmacological activities in cancer and inflammation. However, the ability of tricetin to ameliorate the inflammation that occurs in osteoarthritis (OA) has not been determined. This study explored the effects of tricetin on interleukin- (IL-) 1β-induced rat chondrocytes. Chondrocytes harvested from rat cartilage were incubated in vitro with tricetin in the presence of IL-1β. The expression of matrix metalloproteinase- (MMP-) 1, MMP-3, MMP-13, nitric oxide (NO), prostaglandin E2 (PGE2), Bax, and Bcl-2 was evaluated by real-time-PCR, ELISA, Griess reaction, and western blotting. Caspase-3 activity in chondrocytes was determined using a caspase-3 activity assay and MAPK pathway activity by western blotting. Tricetin decreased the expression of MMP-1, MMP-3, and MMP-13 at both the gene and protein level in IL-1β-induced rat chondrocytes. It also inhibited IL-1β-induced NO and PGE2 production, by modulating inducible NO synthase and cyclooxygenase 2 gene expression. An antiapoptotic role of tricetin involving the Bax/Bcl-2/caspase-3 pathway was also determined. The chondroprotective effect of tricetin was shown to be partly related to the suppression of the MAPK signaling pathway. The results of this study demonstrate the chondroprotective role of tricetin, based on its anticatabolic, anti-inflammatory, and antiapoptotic effects in chondrocytes. The therapeutic potential of tricetin in OA patients should be explored in future studies.

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Section: Resultssupporting

confidence: 90%

Tricetin Protects Rat Chondrocytes against IL-1β-Induced Inflammation and Apoptosis

Sun

Xiong

et al. 2019

Oxidative Medicine and Cellular Longevity

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“…Casticin is a flavonoid extracted from Rhizoma butensis , which has various biological effects such as anti‐tumor, anti‐inflammatory, and improvement of airway responses in asthma 12‐14 . Besides, it has remarkable effects on nuclear factor, erythroid 2‐like 2 (Nrf2), kelch‐like ECH‐associated protein 1 (Keap1), NF‐κB, and other targets of oxidative stress and inflammation 15 .…”

Section: Introductionmentioning

confidence: 99%

Casticin protected against neuronal injury and inhibited the TLR4/NF‐κB pathway after middle cerebral artery occlusion in rats

Huang

Zhou²,

et al. 2021

Pharmacology Res & Perspec

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Although stroke is a major human neurological disease, there is a paucity of effective neuroprotectants that can improve its treatment. Casticin is a natural monomer drug with many biological effects such as anti‐inflammatory and anti‐tumor actions. However, it is not clear whether it has a neuroprotective effect in ischemic stroke. In this study, the neuroprotective effect of casticin in a rat middle cerebral artery occlusion (MCAO) model was investigated. Results showed that casticin reduced the volume of the cerebral infarction, mNSS scores, swimming distance, time to find the submerged platform, and serum concentrations of TNF‐α, TGF‐β, IL‐6 in MCAO rats. Moreover, casticin also decreased the expression of TLR4, NF‐κB p65, and NF‐κB p50 proteins and reversed the reduced expression of IκB protein in the brain tissue of MCAO rats. The in vitro study revealed that casticin decreased apoptosis of OGD/R‐PC12 cells, reduced the expression of TLR4, NF‐κB p65, and NF‐κB p50, while increased IκB protein expression. In conclusion, casticin improved the neurological functions of MCAO rats via inhibiting the TLR4/NF‐κB pathway and might have the potential to be developed into a neuroprotective agent for stroke patients.

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“…It is used for the treatment of premenstrual syndrome (PMS) in European with little adverse effects [19]. Casticin displayed genotoxic or cytotoxic effects on cancer cells at low doses and on normal cells at high doses [31,35]. Recently, casticin was documented to exert potential anti-cancer effects, but the limitation of casticin may be the poor water solubility and the fact that few pharmacokinetic studies are available [36].…”

Section: Discussionmentioning

confidence: 99%

Casticin Induces DNA Damage and Affects DNA Repair Associated Protein Expression in Human Lung Cancer A549 Cells

et al. 2020

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Casticin was obtained from natural plants, and it has been shown to exert biological functions; however, no report concerns the induction of DNA damage and repair in human lung cancer cells. The objective of this study was to investigate the effects and molecular mechanism of casticin on DNA damage and repair in human lung cancer A549 cells. Cell viability was determined by flow cytometric assay. The DNA damage was evaluated by 4’,6-diamidino-2-phenylindole (DAPI) staining and electrophoresis which included comet assay and DNA gel electrophoresis. The protein levels associated with DNA damage and repair were analyzed by western blotting. The expression and translocation of p-H2A.X were observed by confocal laser microscopy. Casticin reduced total viable cell number and induced DNA condensation, fragmentation, and damage in A549 cells. Furthermore, casticin increased p-ATM at 6 h and increased p-ATR and BRCA1 at 6–24 h treatment but decreased p-ATM at 24–48 h, as well as decreased p-ATR and BRCA1 at 48 h. Furthermore, casticin decreased p-p53 at 6–24 h but increased at 48 h. Casticin increased p-H2A.X and MDC1 at 6–48 h treatment. In addition, casticin increased PARP (cleavage) at 6, 24, and 48 h treatment, DNA-PKcs and MGMT at 48 h in A549 cells. Casticin induced the expressions and nuclear translocation of p-H2AX in A549 cells by confocal laser microscopy. Casticin reduced cell number through DNA damage and condensation in human lung cancer A549 cells.

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Casticin protects against IL-1β-induced inflammation in human osteoarthritis chondrocytes

Cited by 25 publications

References 32 publications

Tricetin Protects Rat Chondrocytes against IL-1β-Induced Inflammation and Apoptosis

Tricetin Protects Rat Chondrocytes against IL-1β-Induced Inflammation and Apoptosis

Casticin protected against neuronal injury and inhibited the TLR4/NF‐κB pathway after middle cerebral artery occlusion in rats

Casticin Induces DNA Damage and Affects DNA Repair Associated Protein Expression in Human Lung Cancer A549 Cells

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