Protective effects of Salvianolic acid B on rat ferroptosis in myocardial infarction through upregulating the Nrf2 signaling pathway

Shen, Yuehong; Shen, Xinyu; Zhang, Yunyun; Wang, Yue; Ye, Ding; Shen, Jiayun; Zhao, Jianqiao; Qin, Huahan; Xu, Yuehua; Zhou, Qian; Wang, Xindong; Shen, Jianping

doi:10.1016/j.intimp.2022.109257

Cited by 36 publications

(16 citation statements)

References 43 publications

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“…Furthermore, PLD inhibition reinstated the diminished levels of SOD and reduced GSH under OGD/R conditions, thus bolstering antioxidant efficacy.Notably, ferroptosis emerges as a key form of programmed cell death induced by oxidative stress, driven by an imbalance between ROS production and the cellular capacity to neutralize ROS. The accumulation of iron ions, particularly ferrous ions (Fe2+), is a central trigger, instigating ROS generation via the Fenton reaction, ultimately leading to cellular membrane damage and ferroptosis 23,28,37. Our study uncovers the involvement of PLD1 and PLD2 in ferroptosis regulation.…”

mentioning

confidence: 74%

“…ACSL4 is a limiting factor for lipid peroxidation and essential for ferroptosis initiation. This enzyme plays an essential role in iron‐dependent oxidative stress and is a limiting factor in the conversion of long‐chain fatty acids into acyl‐coenzymes 23,37 . We conducted western blot analysis (Figure 3C), which demonstrated that the expression of GPX4, SLC7A11, and FTH1 decreased concurrently after OGD/R, while the expression of ACSL4 increased.…”

Section: Resultsmentioning

confidence: 99%

“…Additionally, the inhibition of PLD1 or PLD2 was identified as an effective approach to decrease OGD/R-induced ferroptosis (Figure 3A,B conversion of long-chain fatty acids into acyl-coenzymes. 23,37 We conducted western blot analysis (Figure 3C), which demonstrated that the expression of GPX4, SLC7A11, and FTH1 decreased concurrently after OGD/R, while the expression of ACSL4 increased. However, treatment with PLD1i or PLD2i and si-PLD1 or si-PLD2 increased the expression of GPX4, SLC7A11, and FTH1 and decreased the expression of ACSL4.…”

Section: Blocking Pld1 or Pld2 Can Mitigate The Ferroptosis Caused By...mentioning

confidence: 99%

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OGD/R‐induced ferroptosis and pyroptosis in retinal pigment epithelium cells: Role of PLD1 and PLD2 modulation

Park,

Kang,

Park

et al. 2023

Cell Biochemistry & Function

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This study investigated the role of phospholipase D (PLD) in retinal ischemia–reperfusion (I/R) injury using an oxygen‐glucose deprivation/reperfusion (OGD/R) model commonly used in retinal I/R injury research. To create an in vitro cellular I/R model, pharmacological inhibitors and small interfering RNA (siRNA) were used to target PLD1 and PLD2 in retinal pigment epithelial (RPE) cells. Treatment with PLD inhibitors and siRNA reduced reactive oxygen species (ROS) and malondialdehyde (MDA) induced by OGD/R in RPE cells and increased the levels of superoxide dismutase (SOD) and glutathione (GSH), indicating a reduction in oxidative damage and improvement in the antioxidant system. Next, we showed that inhibiting PLD1 or PLD2 reduced intracellular iron levels and lipid peroxidation, which are critical factors in ferroptosis. Additionally, PLD1 and PLD2 modulated the expression of proteins involved in the regulation of ferroptosis, including GPX4, SLC7A11, FTH1, and ACSL4. We also investigated the roles of PLD1 and PLD2 in preventing pyroptosis, another form of programmed cell death associated with inflammation. Our study found that OGD/R significantly increased the production of pro‐inflammatory cytokines and activated caspase‐1, NLRP3, ASC, cleaved‐caspase 1 (C‐caspase‐1), and GSDMD‐N in RPE cells, indicating pyroptosis induction. However, PLD1 and PLD2 inhibition or knockdown significantly inhibited the production of pro‐inflammatory cytokines and activation of the NLRP3 inflammasome, Taken together, our findings support the hypothesis that the PLD signaling pathway plays a key role in OGD/R‐induced ferroptosis and pyroptosis induction and may be a potential therapeutic target for preventing or treating retinal dysfunction and degeneration.

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confidence: 74%

Section: Resultsmentioning

confidence: 99%

Section: Blocking Pld1 or Pld2 Can Mitigate The Ferroptosis Caused By...mentioning

confidence: 99%

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OGD/R‐induced ferroptosis and pyroptosis in retinal pigment epithelium cells: Role of PLD1 and PLD2 modulation

Park,

Kang,

Park

et al. 2023

Cell Biochemistry & Function

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“…Considering cell death pathways, apart from apoptosis, it is also relevant to mention an in vivo study using SAB (25–50 mg/kg) administered to Sprague Dawley rats, in which SAB was able to prevent ferroptosis in a model of myocardial infarction, confirmed through increased expression of ferroptosis biomarkers cystine/glutamate transporter (xCT), glutathione peroxidase 4, ferroportin 1 (FPN1) and ferritin heavy chain (FTH1) when compared to animals with myocardial infarction [ 115 ].…”

Section: Modulation Of Cell Survival and Cell Death Pathways By Phyto...mentioning

confidence: 99%

Modulation of Cell Death Pathways for Cellular Protection and Anti-Tumoral Activity: The Role of Thymus spp. Extracts and Their Bioactive Molecules

Martins-Gomes

Nunes

Silva

2023

IJMS

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Natural products used for their health-promoting properties have accompanied the evolution of humanity. Nowadays, as an effort to scientifically validate the health-promoting effects described by traditional medicine, an ever-growing number of bioactivities are being described for natural products and the phytochemicals that constitute them. Among them, medicinal plants and more specifically the Thymus genus spp., arise as products already present in the diet and with high acceptance, that are a source of phytochemicals with high pharmacological value. Phenolic acids, flavonoid glycoside derivatives, and terpenoids from Thymus spp. have been described for their ability to modulate cell death and survival pathways, much-valued bioactivities in the pharmaceutical industry, that continually sought-after new formulations to prevent undesired cell death or to control cell proliferation. Among these, wound treatment, protection from endogenous/exogenous toxic molecules, or the induction of selective cell death, such as the search for new anti-tumoral agents, arise as main objectives. This review summarizes and discusses studies on Thymus spp., as well as on compounds present in their extracts, with regard to their health-promoting effects involving the modulation of cell death or survival signaling pathways. In addition, studies regarding the main bioactive molecules and their cellular molecular targets were also reviewed. Concerning cell survival and proliferation, Thymus spp. present themselves as an option for new formulations designed for wound healing and protection against chemicals-induced toxicity. However, Thymus spp. extracts and some of their compounds regulate cell death, presenting anti-tumoral activity. Therefore Thymus spp. is a rich source of compounds with nutraceutical and pharmaceutical value.

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“…It is frequently used to prevent cardiac dysfunction diseases such as atherosclerosis, myocardial cell injury, myocardial hypertrophy, and myocardial infarction. By controlling the Nrf2 signaling pathway, reducing lipid peroxide accumulation and mitochondrial damage, regulating the expression of myocardial iron homeostasis proteins and oxidative stress reactions, and inhibiting ferroptosis, it can significantly decrease myocardial injury in rats with myocardial infarction [ 106 – 108 ]. Last but not least, geniposide, an active compound mostly obtained from Gardenia jasminoides Ellis, exhibits anti-inflammatory, antioxidant, antithrombotic, and ameliorative effects on the disturbance of glucose and lipid metabolism.…”

Section: Effects Of Ferroptosis On Cardiovascular Diseasementioning

confidence: 99%

Effects of Ferroptosis on Cardiovascular Diseases

Zhang

et al. 2023

Mediators of Inflammation

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Ferroptosis is a novel form of programmed cell death characterized by the accumulation of iron-dependent lipid peroxides, which causes membrane injury. Under the catalysis of iron ions, cells deficient in glutathione peroxidase (GPX4) cannot preserve the balance in lipid oxidative metabolism, and the buildup of reactive oxygen species on the membrane lipids leads to cell death. An increasing body of evidence suggests that ferroptosis plays a significant role in the development and occurrence of cardiovascular diseases. In this paper, we mainly elaborated on the molecular mechanisms regulating ferroptosis and its impact on cardiovascular disease to lay the groundwork for future studies on the prophylaxis and treatment of this patient population.

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Protective effects of Salvianolic acid B on rat ferroptosis in myocardial infarction through upregulating the Nrf2 signaling pathway

Cited by 36 publications

References 43 publications

OGD/R‐induced ferroptosis and pyroptosis in retinal pigment epithelium cells: Role of PLD1 and PLD2 modulation

OGD/R‐induced ferroptosis and pyroptosis in retinal pigment epithelium cells: Role of PLD1 and PLD2 modulation

Modulation of Cell Death Pathways for Cellular Protection and Anti-Tumoral Activity: The Role of Thymus spp. Extracts and Their Bioactive Molecules

Effects of Ferroptosis on Cardiovascular Diseases

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