Schisandrin A from Schisandra chinensis Attenuates Ferroptosis and NLRP3 Inflammasome-Mediated Pyroptosis in Diabetic Nephropathy through Mitochondrial Damage by AdipoR1 Ubiquitination

Wang, Xiaohu; Li, Qin; Sui, Bangzhi; Xu, Maodi; Pu, Zhichen; Qiu, Teng

doi:10.1155/2022/5411462

Cited by 32 publications

(22 citation statements)

References 52 publications

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“…At present, studies have found that there are three main ways to participate in the mechanism of iron death. First, iron metabolism pathway [36]. This is a phospholipid lipid peroxidation pathway mediated by oxidative stress, iron and enzymes.…”

Section: Discussionmentioning

confidence: 99%

APOC1 reduced anti-PD-1 immunotherapy of nonsmall cell lung cancer via the transformation of M2 into M1 macrophages by ferroptosis by NRF2/HO-1

Mei,

Long,

et al. 2024

Anti-Cancer Drugs

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The treatment strategy for nonsmall cell lung cancer (NSCLC) has always been a hot topic of concern, and its treatment strategies are also emerging. This experiment wants to know the effects of apolipoprotein C1 (APOC1) in immunotherapy of NSCLC. APOC1 mRNA and protein expression were upregulated in lung cancer tissue of patients with NSCLC. programmed cell death protein 1 (PD-1) mRNA expression was negatively correlated with PD-1 mRNA expression in patients. The survival rate of APOC1 high expression was lower than that of low expression in patients with NSCLC. APOC1 gene reduced the transformation of M2 into M1 macrophages (TMMM). APOC1 gene promoted cell growth, and the gene reduced ferroptosis of NSCLC. APOC1-induced nuclear factor erythroid 2-related factor 2/heme oxygenase-1 (NRF2/HO-1) signaling pathway. Sh-APOC1 gene reduced cell growth in mice of NSCLC through the inhibition of NRF2/HO-1 signaling pathway. The inhibition of NRF2 reduced the TMMM by APOC1. The activation of NRF2 reduced the TMMM by si-APOC1. In conclusion, APOC1 reduced anti-PD-1 immunotherapy of NSCLC via the TMMM by ferroptosis by NRF2/HO-1, suggesting that targeting this mechanism of APOC1 may be a feasible strategy for anti-PD-1 immunotherapy for NSCLC.

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Section: Discussionmentioning

confidence: 99%

APOC1 reduced anti-PD-1 immunotherapy of nonsmall cell lung cancer via the transformation of M2 into M1 macrophages by ferroptosis by NRF2/HO-1

Mei,

Long,

et al. 2024

Anti-Cancer Drugs

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“…It is well known that Deo has a strong anti-inflammatory effect in various inflammatory diseases, such as diabetes, kidney disease, and cardiovascular disease, and is significantly related to the treatment and prognosis of these diseases. 29–31 Relevant studies also indicate that Deo has an effect in the treatment of inflammation. For example, Deo can treat ulcerative colitis through the TLR4/NF-κB signal pathway.…”

Section: Discussionmentioning

confidence: 99%

Deoxyschizandrin Inhibits PTEN to Regulate Inflammation in Doxorubicin-induced Hepatotoxicity

Wang

Zhou

2023

Pharmacognosy Magazine

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Aim Doxorubicin (DOX) has long been criticized for its cardiotoxicity, yet one cannot overlook its hepatotoxicity. Deoxyschizandrin (Deo) is a type of monomer used in traditional Chinese medicine that has a powerful anti-inflammatory action and is frequently used to treat a variety of inflammatory diseases. However, its therapeutic effect on DOX-induced hepatotoxic inflammatory reactions is still unknown. Materials and Methods In this study, DOX was used to induce hepatotoxicity in rats, and the effects of Deo on hepatotoxicity and hepatic inflammation were investigated. Results The results show that Deo protects liver function by inhibiting PETN, which regulates DOX-induced liver inflammation. Conclusion The anti-inflammatory effect of Deo in DOX-induced hepatotoxicity is attributed to the inhibition of phosphatase and tensin homolog deleted on chromosome ten (PTEN) and the increase in AKT phosphorylation.

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“…Pyroptosis can be divided into classical death pathway that depends on NLRP3 inflammatory vesicles and caspase-1, and the non-classical death pathway that depends on caspase-4 /5/11 [33]. In addition, pyroptosis can be described by pore formation on the membrane due to gasdermin, cell swelling and rapid lysis, and subsequent several pro-inflammatory mediators interleukin-1β (IL-1β) and interleukin-18 (IL-18) release [33][34][35]. Plenty of studies have demonstrated that pyroptosis is implicated with many diseases, such as atherosclerotic diseases, metabolic diseases, and aseptic inflammatory diseases of important organs [33,36,37].…”

Section: Discussionmentioning

confidence: 99%

Ceramide induces pyroptosis through TXNIP/NLRP3/GSDMD pathway in HUVECs

Liu

Zhang

Shi

et al. 2022

BMC Mol and Cell Biol

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Background Pyroptosis of endothelial cells is a new cause of endothelial dysfunction in multiple diseases. Ceramide acts as a potential bioactive mediator of inflammation and increases vascular endothelial permeability in many diseases, whether it can aggravate vascular endothelial injury by inducing cell pyroptosis remains unknown. This study was established to explore the effects of C8-ceramide (C8-Cer) on human umbilical vein vascular endothelial cells (HUVECs) and its possible underlying mechanism. Methods HUVECs were exposed to various concentrations of C8-Cer for 12 h, 24 h, 48 h. The cell survival rate was measured using the cell counting kit-8 assay. Western blotting and Real-time polymerase chain reaction (RT-PCR) were used to detect the pyroptosis-releated protein and mRNA expressions, respectively. Caspase-1 activity assay was used to detect caspase-1 activity. Hoechst 33342/propidium iodide double staining and flow cytometry were adopted to measure positive staining of cells. Lactate dehydrogenase release assay and enzyme-linked immunosorbent assay were adopted to measure leakage of cellular contents. FITC method was used to detect the permeability of endothelial cells. ROS fluorescence intensity were detected by flow cytometry. Results The viability of HUVECs decreased gradually with the increase in ceramide concentration and time. Ceramide upregulated the expression of thioredoxin interacting protein (TXNIP), NLRP3, GSDMD, GSDMD-NT, caspase-1 and Casp1 p20 at the protein and mRNA level in a dose-dependent manner. It also enhanced the PI uptake in HUVECs and upregulated caspase-1 activity. Moreover, it promoted the release of lactate dehydrogenase, interleukin-1β, and interleukin-18. Meanwhile, we found that ceramide led to increased vascular permeability. The inhibitor of NLRP3 inflammasome assembly, MCC950, was able to disrupt the aforementioned positive loop, thus alleviating vascular endothelial cell damage. Interestingly, inhibition of TXNIP either chemically using verapamil or genetically using small interfering RNA (siRNA) can effectively inhibit ceramide-induced pyroptosis and improved cell permeability. In addition, ceramide stimulated reactive oxygen species (ROS) generation. The pretreatment of antioxidant N-acetylcysteine (NAC), ROS scavenger, blocked the expression of pyroptosis markers induced by C8-cer in HUVECs. Conclusion The current study demonstrated that C8-Cer could aggravate vascular endothelial cell damage and increased cell permeability by inducing cell pyroptosis. The results documented that the ROS-dependent TXNIP/NLRP3/GSDMD signalling pathway plays an essential role in the ceramide-induced pyroptosis in HUVECs.

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Schisandrin A from Schisandra chinensis Attenuates Ferroptosis and NLRP3 Inflammasome-Mediated Pyroptosis in Diabetic Nephropathy through Mitochondrial Damage by AdipoR1 Ubiquitination

Cited by 32 publications

References 52 publications

APOC1 reduced anti-PD-1 immunotherapy of nonsmall cell lung cancer via the transformation of M2 into M1 macrophages by ferroptosis by NRF2/HO-1

APOC1 reduced anti-PD-1 immunotherapy of nonsmall cell lung cancer via the transformation of M2 into M1 macrophages by ferroptosis by NRF2/HO-1

Deoxyschizandrin Inhibits PTEN to Regulate Inflammation in Doxorubicin-induced Hepatotoxicity

Ceramide induces pyroptosis through TXNIP/NLRP3/GSDMD pathway in HUVECs

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