Cedrol alleviates the apoptosis and inflammatory response of IL-1β-treated chondrocytes by promoting miR-542-5p expression

Dong, Wang-chao; Wang, Shanshan; Qian, Weiqing; Li, Suming; Wang, Peimin

doi:10.1007/s11626-021-00620-3

Cited by 3 publications

(3 citation statements)

References 47 publications

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“… 36 , 37 In addition, IL‐1β, as one of the IL‐1 family of cytokines members, draws a significant impact on inflammatory responses and is involved in cell proliferation, differentiation, and apoptosis. 38 What's more, some other research reported that Scutellarin significantly attenuated the expression of inflammatory, apoptosis factors. 39 In our study, we also reported that Scutellarin is able to downregulate the expression of caspase 3, caspase 7, and IL‐1β.…”

Section: Discussionmentioning

confidence: 98%

“…Some studies found that the levels of caspase 3 and caspase 7 were aberrantly activated in both cortices and hippocampi following HI 36,37 . In addition, IL‐1β, as one of the IL‐1 family of cytokines members, draws a significant impact on inflammatory responses and is involved in cell proliferation, differentiation, and apoptosis 38 . What's more, some other research reported that Scutellarin significantly attenuated the expression of inflammatory, apoptosis factors 39 .…”

Section: Discussionmentioning

confidence: 99%

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Scutellarin protects cortical neurons against neonatal hypoxic‐ischemic encephalopathy injury via upregulation of vascular endothelial growth factor

Zou

Fang

Wang

et al. 2022

Ibrain

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Neonatal hypoxic-ischemic encephalopathy (NHIE) causes devastating cerebral damage and neurological deficits that seldom have effective therapies.This study aimed to explore the mechanisms underlying the therapeutic efficacy of Scutellarin in NHIE. NHIE models were successfully established.Zea-longa score and triphenyte-trazoliumchloride (TTC) staining demonstrated that hypoxia and ischemia (HI) insult induced prominent neurological dysfunctions and brain infarction. Protein microarray was applied to detect the differentially expressed genes in the cortex, hippocampus, and lung tissues of HI rats, which revealed the downregulation of vascular endothelial growth factor (VEGF) in these tissues. Additionally, double immunostaining uncovered VEGF expression was localized in the neurons. Besides, VEGF was decreasingly expressed in oxygen-glucose deprivation (OGD) neurons, which was intriguingly reversed by Scutellarin treatment. Moreover, VEGF silencing increased OGD-induced neuronal apoptosis and attenuated neurite outgrowth, which was enhanced by Scutellarin administration. GeneMANIA predicted a close correlation of VEGF with caspase 3, caspase 7, and interleukin (IL)-1β, and qRT-PCR revealed that Scutellarin treatment depressed the expression levels of them elevated in OGD neurons, but the Scutellarin-depressed levels of these factors were prominently increased after VEGF silencing. Our findings suggested that Scutellarin exerted neuroprotective effects in NHIE potentially through mediating VEGF-targeted inactivation of caspase 3, caspase 7, and IL-1β.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Scutellarin protects cortical neurons against neonatal hypoxic‐ischemic encephalopathy injury via upregulation of vascular endothelial growth factor

Zou

Fang

Wang

et al. 2022

Ibrain

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“…44 Whether tested in vivo or in vitro, IL-1β, being one of the essential proinflammatory cytokines, leads to cartilage cell apoptosis, cartilage matrix degradation, and joint inflammation, thereby promoting OA progression. 45,46 For this reason, a model of in vitro OA simulated by IL-1β was used in this study. Our present leads indicate that the mRNA of PKC-δ increases following IL-1β application to rat chondrocytes and the protein levels of both PKC-δ and p-PKC -δ increase in dose-dependent ways.…”

Section: Discussionmentioning

confidence: 99%

PKC-δ Promotes IL-1β-Induced Apoptosis of Rat Chondrocytes and Via Activating JNK and P38 MAPK Pathways

Lü

2023

CARTILAGE

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Objective Protein kinase C-delta (PKC-δ) is involved in apoptosis. This study aimed to establish whether PKC-δ can further promote IL-1β-induced chondrocyte apoptosis by mediating the phosphorylation of the JNK and p38 mitogen-activated protein kinase (MAPK) signaling pathways In osteoarthritis (OA). Methods We employed chondrocyte staining to determine the extent of cartilage degeneration. PKC-δ and p38 signal expressions were used in the immunohistochemical (IHC) test and apoptosis was assayed at the TUNEL test in human osteoarthritic and controls. We stimulated rat cartilage cells using IL-1β (10 ng/ml)/rottlerin (10 μM) or lentivirus. To determine the apoptosis rate, we employed flow cytometry. The mRNA of both BCL2-related X (BAX) and cysteine aspartate protease 3 (caspase-3) could be measured via qRT-PCR. Western blot measured the protein levels of BAX, caspase-3, PKC-δ, p-JNK/JNK and p-p38/p38. Results The positive rate of PKC-δ and the apoptotic rate of chondrocytes in OA were higher than controls. The manifestation of PKC-δ was positively related to the degree of cartilage degeneration, p38 protein expression, and apoptosis rate. IL-1β exposure upregulated PKC-δ expression in chondrocytes in a dose-dependent manner. Decreasing PKC-δ expression and its phosphorylation in OA can inhibit MAPK signaling pathway activation (phosphorylation) by downregulating JNK and p38 protein phosphorylation and expression. This inhibition decreases caspase-3 and BAX levels, consequently lowering the apoptosis rate in chondrocytes. Conclusion PKC-δ activation by IL-1β in OA promotes chondrocyte apoptosis via activation of the JNK and p38 MAPK signal pathways, thereby promoting the OA progression.

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Cardioprotective effect of cedrol in an inflammation systemic model induced by lipopolysaccharide: Biochemical and histological verification

Rastegar-Moghaddam,

Amirahmadi,

Akbarian

et al. 2024

J Cardiovasc Thorac Res

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Introduction: Evidence declared lipopolysaccharide (LPS) initiates inflammatory responses by stimulating the abandon of cytokines, which may perturb organ function. On the other side, it has been suggested Cedrol has potential properties, including anti-inflammatory and anti-oxidative activities. Herein, this study was done to assess the protective effect of Cedrol against LPS-associated heart damage. Methods: Thirty-five rats (200-250 g) were sorted into five groups, including control, LPS, LPS-Cedrol 7.5 mg/kg, LPS-Cedrol 15 mg/kg, and LPS-Cedrol 30 mg/kg groups. Cedrol was administrated through injected intra-peritoneally for two weeks. The heart tissues were removed and malondialdehyde (MDA) as a lipid peroxidation marker, superoxide dismutase (SOD), and catalase (CAT) as antioxidant markers were assessed. Furthermore, the interleukin (IL)-6 level in cardiac tissue was measured and Masson’s trichrome methods were employed to appraise cardiac inflammation and fibrosis, respectively. Results: Inflammation induced by LPS was significantly accompanied by myocardial fibrosis which was shown by Masson’s trichrome staining (P<0.001). In addition, LPS administration enhanced the MDA level while it diminished the activity of anti-oxidant markers such as CAT and SOD (P<0.001 for all cases). In the histological results, Cedrol improved LPS-induced inflammation and cardiac fibrosis (P<0.01 to P<0.001). Cedrol also enhanced CAT and SOD activities, whereas declined MDA level in the cardiac tissue (P<0.01 to P<0.001). Conclusion: The current findings proposed that the administration of Cedrol exerted a protective role in LPS-associated heart damage by reducing inflammation, cardiac fibrosis, and oxidative stress.

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Cedrol alleviates the apoptosis and inflammatory response of IL-1β-treated chondrocytes by promoting miR-542-5p expression

Cited by 3 publications

References 47 publications

Scutellarin protects cortical neurons against neonatal hypoxic‐ischemic encephalopathy injury via upregulation of vascular endothelial growth factor

Scutellarin protects cortical neurons against neonatal hypoxic‐ischemic encephalopathy injury via upregulation of vascular endothelial growth factor

PKC-δ Promotes IL-1β-Induced Apoptosis of Rat Chondrocytes and Via Activating JNK and P38 MAPK Pathways

Cardioprotective effect of cedrol in an inflammation systemic model induced by lipopolysaccharide: Biochemical and histological verification

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