Ameliorative effect of rosiglitazone, a peroxisome proliferator gamma agonist on adriamycin‐induced cardio toxicity via suppressing oxidative stress and apoptosis

Zhang, Lingling; Wu, Po-Liang; Zhang, Luyan; Sreeharsha, Nagaraja; Mishra, Anurag; Su, Xinyou

doi:10.1002/iub.2190

Cited by 7 publications

(3 citation statements)

References 47 publications

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“…Ferroptosis has been reported to be associated with damage to the brain and heart. 15,16 Thiazolidinediones appear to work preventively rather than therapeutically, under this condition, we injected rosiglitazone into the abdominal cavity 30 min before the operation, 30 min after the operation and 4 h after the operation, thus allowing sufficient time for proper phospholipid remodelling. The results showed that intraperitoneal injection of rosiglitazone reduced brain edema and ROS accumulation in SBI rats (Figure 2C).…”

Section: Discussionmentioning

confidence: 99%

Rosiglitazone inhibits acyl‐CoA synthetase long‐chain family number 4 and improves secondary brain injury in a rat model of surgical brain injury

Shen,

Qian,

et al. 2023

Clin Exp Pharma Physio

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Ferroptosis is a recently discovered non‐apoptotic form of cellular death. Acyl‐CoA synthetase long‐chain family number 4 (ACSL4) is necessary for iron‐dependent cellular death, and reactive oxygen species (ROS) produced by ACSL4 are the executioners of ferroptosis. Rosiglitazone improves ferroptosis by inhibiting ACSL4. There is no research indicating whether ACSL4 plays a role in cell death after surgical brain injury (SBI). This study aimed to investigate the role of ACSL4 in SBI via the ferroptosis pathway. Ninety male Sprague–Dawley rats were examined using a model of SBI. Subsequently, the inhibitory effect of rosiglitazone on ACSL4 was assessed via western blot, real‐time polymerase chain reaction (PCR), immunofluorescence, fluoro‐jade C staining, Perl's staining, ROS assay, and neurological scoring. The results showed that compared with the Sham group, the protein levels of ACSL4 and transferrin were significantly increased after SBI. Administration of rosiglitazone significantly reduced neuronal necrosis, iron deposition, brain water content and ROS in brain tissue and ameliorated neurological deficits at 48 h after SBI, which was concomitant with decreased transferrin expression. These findings demonstrate that SBI‐induced upregulation of ACSL4 may be partly mediated by the ferroptosis pathway, which can be reversed by rosiglitazone administration.

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Section: Discussionmentioning

confidence: 99%

Rosiglitazone inhibits acyl‐CoA synthetase long‐chain family number 4 and improves secondary brain injury in a rat model of surgical brain injury

Shen,

Qian,

et al. 2023

Clin Exp Pharma Physio

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“…Rosiglitazone and pioglitazone belong to the thiazolidinedione class of hypoglycemic agents and are recognized as PPAR-γ agonists. These two drugs were not only able to enrich GSH contents and GPX activity and defend the heart against oxidative stress but also prevented DOX or I/R-induced myocardial injury [214][215][216][217]. Some clinical studies have shown that pioglitazone treatment (30 mg/day, P.O for 4 weeks) exhibits antioxidant properties in diabetic patients, as reflected by a decrease in MDA [218,219].…”

Section: Glutathione System Activatormentioning

confidence: 99%

Glutathione system enhancement for cardiac protection: pharmacological options against oxidative stress and ferroptosis

Tan

Yin

et al. 2023

Cell Death Dis

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The glutathione (GSH) system is considered to be one of the most powerful endogenous antioxidant systems in the cardiovascular system due to its key contribution to detoxifying xenobiotics and scavenging overreactive oxygen species (ROS). Numerous investigations have suggested that disruption of the GSH system is a critical element in the pathogenesis of myocardial injury. Meanwhile, a newly proposed type of cell death, ferroptosis, has been demonstrated to be closely related to the GSH system, which affects the process and outcome of myocardial injury. Moreover, in facing various pathological challenges, the mammalian heart, which possesses high levels of mitochondria and weak antioxidant capacity, is susceptible to oxidant production and oxidative damage. Therefore, targeted enhancement of the GSH system along with prevention of ferroptosis in the myocardium is a promising therapeutic strategy. In this review, we first systematically describe the physiological functions and anabolism of the GSH system, as well as its effects on cardiac injury. Then, we discuss the relationship between the GSH system and ferroptosis in myocardial injury. Moreover, a comprehensive summary of the activation strategies of the GSH system is presented, where we mainly identify several promising herbal monomers, which may provide valuable guidelines for the exploration of new therapeutic approaches.

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“…Studies have shown that RGZ has both insulin-sensitizing effects and anti-in ammatory and immune-modulating effects. RGZ plays its anti-in ammatory roles in the acute and chronic in ammatory responses of many organs such as the heart, lung, kidney, and gastrointestinal tract [11][12][13][14]. Bo et al reported that RGZ pretreatment alleviated LPS-induced placental in ammation and reduced embryonic mortality in mice [15].…”

Section: Introductionmentioning

confidence: 99%

Rosiglitazone alleviates LPS-induced endometritis via suppression of TLR4-mediated NF-κB activation

Bao

Cong

et al. 2022

Preprint

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Endometritis is a common reproductive system disease that seriously affects the reproductive health of women of childbearing age. Rosiglitazone (RGZ) is known to have anti-inflammatory and immunomodulatory effects. The effect of RGZ on the treatment of endometritis has not been reported. In the present study, we aimed to investigate the anti-inflammatory effect of RGZ on lipopolysaccharide (LPS)-induced endometritis and to explore its possible mechanism of action. Using LPS-induced endometritis mice as a model, the preventive and therapeutic effects of RGZ on endometrial inflammation were explored. Histopathology revealed that RGZ significantly attenuated LPS-induced endometritis in C57BL/6 mice. The anti-inflammatory effects of RGZ and possible related signaling pathways were investigated in vitro using human endometrial stromal cells (HESCs). The results of reverse transcription-polymerase chain reaction and western blot analysis showed that RGZ pretreatment could inhibit the expression of Toll-like receptor 4 (TLR4) and its downstream activation of nuclear factor-κB (NF-κB). Collectively, these results suggest that RGZ may inhibit LPS-induced endometritis through the TLR4-mediated NF-κB pathway.

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Ameliorative effect of rosiglitazone, a peroxisome proliferator gamma agonist on adriamycin‐induced cardio toxicity via suppressing oxidative stress and apoptosis

Cited by 7 publications

References 47 publications

Rosiglitazone inhibits acyl‐CoA synthetase long‐chain family number 4 and improves secondary brain injury in a rat model of surgical brain injury

Rosiglitazone inhibits acyl‐CoA synthetase long‐chain family number 4 and improves secondary brain injury in a rat model of surgical brain injury

Glutathione system enhancement for cardiac protection: pharmacological options against oxidative stress and ferroptosis

Rosiglitazone alleviates LPS-induced endometritis via suppression of TLR4-mediated NF-κB activation

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