Protective effects of apigenin against 3-MCPD-induced renal injury in rat

Zhong, Yujie; Jin, Chengni; Wang, Xiaorui; Li, Xuan; Han, Jiahui; Wei, Xue; Wu, Peng; Peng, Xiaoli; Xia, Xiaodong

doi:10.1016/j.cbi.2018.08.005

Cited by 24 publications

(11 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Zhong et al found that apigenin can alleviate 3-MCPD-induced renal injury in rats by regulating mitochondrial oxidative phosphorylation and endogenous apoptosis of caspase through the gavage of apigenin in rats. 106 Subsequently, they also found that diosgenin can protect against 3-MCPD-induced renal injury by inducing autophagy and improving mitochondrial fission and fusion through the LKB1-AMPK-mTOR pathway. 107 In another research, cyanidin-3-O-glucoside exhibited a protective effect against 3-MCPD-induced intestinal injury and testicular injury in rats.…”

Section: ■ Trends In Future Studymentioning

confidence: 99%

“…Recently, researchers have started to explore nutrition interventions to reduce the health risks of 3-MCPDE. Zhong et al found that apigenin can alleviate 3-MCPD-induced renal injury in rats by regulating mitochondrial oxidative phosphorylation and endogenous apoptosis of caspase through the gavage of apigenin in rats . Subsequently, they also found that diosgenin can protect against 3-MCPD-induced renal injury by inducing autophagy and improving mitochondrial fission and fusion through the LKB1-AMPK-mTOR pathway .…”

Section: Trends In Future Studymentioning

confidence: 99%

See 1 more Smart Citation

Bibliometric Analysis of Research Trends on 3-Monochloropropane-1,2-Diol Esters in Foods

Wei

Liu

Zheng

et al. 2022

J. Agric. Food Chem.

View full text Add to dashboard Cite

3-Monochloropropane-1,2-diol esters (3-MCPDE) are common food contaminants mainly formed in the edible oil refining process. Due to their potential hazards, 3-MCPDE has become a widespread food safety concern. In this study, CiteSpace and VOSviewer were used to conduct a bibliometric analysis on the 3-MCPDE research papers collected in the Web of Science Core Collection from 1998 to 2022. The results showed that the number of research publications on 3-MCPDE has increased rapidly since 2010. Analysis of the hotspots in 3-MCPDE studies showed that more attention has been paid to the exposure assessment, formation mechanism, detection methods, mitigation methods and toxicity, and toxicology of 3-MCPDE. Finally, the future trends of research on 3-MCPDE were analyzed and proposed. The mitigation methods and toxicology studies of 3-MCPDE are still the research hotspots in the future. In addition, nutritional intervention for 3-MCPDE toxicity will be an emerging trend.

show abstract

Section: ■ Trends In Future Studymentioning

confidence: 99%

Section: Trends In Future Studymentioning

confidence: 99%

Bibliometric Analysis of Research Trends on 3-Monochloropropane-1,2-Diol Esters in Foods

Wei

Liu

Zheng

et al. 2022

J. Agric. Food Chem.

View full text Add to dashboard Cite

show abstract

“…Based on previous studies, chronic exposure with 3‐MCPD is associated with increasing in ROS level, mitochondrial membrane permeability transition pore opening followed by programmed cell death signaling activation (Gao et al., 2017; Mossoba et al., 2020; Zhong et al., 2018). Therefore, following chronic 3‐MCPD exposure, the amount of IL‐18 as an IFN‐γ‐ prompting element, increases in kidney, leading to the adjustment of IL‐18 precursor matured by caspase‐1 (Bhargava & Schnellmann, 2017; Mei et al., 2017).…”

Section: Introductionmentioning

confidence: 97%

The role of PGC‐1α and metabolic signaling pathway in kidney injury following chronic administration with 3‐MCPD as a food processing contaminant

et al. 2021

View full text Add to dashboard Cite

3‐Monochloropropane‐1,2‐diol (3‐MCPD) as a byproduct of food processing and a carcinogenic agent has attracted much attention in the last decades. Kidney is the main target organ that is sensitive to the toxicity of 3‐MCPD. Due to limited evidence about possible 3‐MCPD toxicity, we design an investigation to determine the role of mitochondrial biogenesis following chronic oral administration of 3‐MCPD (2, 4, 8 and 32 mg/kg) for 2 months in male C57 mice. The present study evaluated the affects of 3‐MCPD in modulating metabolic signalling which is associated with Il‐18, PGC‐1α, Nrf‐2 and Sir3 which are the major transcription factors. Our data confirms controversial behaviors after chronic exposure with 3‐MCPD. Over expression of the PGC‐1α and Sir3 and IL‐18 were observed after exposure with 2,4 & 8 mg kg−1 day−1 of 3‐MCPD. In front, PGC‐1α down‐regulation occurs at the highest dose (32 mg/kg) resulted in kidney injury. Based on the findings, PGC‐1α plays an important role in the restoration of the mitochondrial function during the recovery from chronic kidney injury. We suggest that the PGC‐1α can be consider as a therapeutic target in prevention and treatment of kidney injury after chronic exposure of 3‐MCPD. Practical applications 3‐Monochloropropane‐1, 2‐diol (3‐MCPD) existed in several foods, can induce nephrotoxicity, progressive nephropathy and renal tubule dilation following acute and chronic exposure. It revealed that 3‐MCPD toxicity is related to metabolites which can cause oxidative stress and activation of cell death signaling. It seems that cytotoxicity of 3‐MCPD has disruptive effect on kidney cells due to rise in ROS production and decrease in mitochondrial membrane permeability. These effects can lead to MPT pore opening, cytochrome c release and activation of programed cell death signaling pathway. Therefore, present study was investigated the role of PGC‐1a and the metabolic signaling involved in 3‐MCPD‐induced nephrotoxicity for the first time. Our data revealed that up‐regulation of mitochondrial biogenesis following chronic exposure with 3‐MCPD accelerates recovery of mitochondrial and cellular function in kidney by deacetylation of histones, overexpression of transcription factors (PGC‐1α, Nrf‐2, and Sir3) and maintaining cellular homeostasis.

show abstract

“…The pharmacological versatility of apigenin, for example, antioxidant, neuroprotective, anti-inflammatory, antidiabetic, blood pressure-lowering, and antimicrobial properties have been wellreported (Ali et al, 2017;Nabavi et al, 2018). The phyto-compound has also demonstrated tissue-protective actions against toxicities induced by many xenobiotics and chemotherapeutic drugs (He et al, 2016;Liu et al, 2018;Wu et al, 2021;Zhong et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Reactive oxygen species: Key players in the anticancer effects of apigenin?

Oyenihi

Alabi

et al. 2022

Journal of Food Biochemistry

View full text Add to dashboard Cite

Reactive oxygen species (ROS) exhibit a double-edged sword in cancer-hence their modulation has been an attractive strategy in cancer prevention and therapy. The abundance of scientific information on the pro-oxidant effects of apigenin in cancer cells suggests the crucial role of ROS in its mechanisms of action. Although apigenin is known to enhance the cellular ROS levels to cytotoxic degrees in cancer cells in vitro, it remains to be determined if these pro-oxidant effects prevail or are relevant in experimental tumor models and clinical trials. Here, we critically examine the prooxidant and antioxidant effects of apigenin in cancer to provide insightful perspectives on the association between its ROS-modulating action and anticancer potential.We also discussed these effects in a cell/tissue type-specific context to highlight the factors influencing the switch between antioxidant and pro-oxidant effects. Finally, we raised some questions that need addressing for the potential translation of these studies into clinical applications. Further research into this duality in oxidant actions of apigenin, especially in vivo, may enable better exploitation of its anticancer potential.Practical application: Apigenin is a naturally occurring compound found in chamomile flowers, parsley, celery, peppermint, and citrus fruits. Many human trials of dietary interventions with apigenin-containing herbs and flavonoid mixture on oxidative stress markers, for instance, point to their antioxidant effects and health benefits in many diseases. Preclinical studies suggest that apigenin alone or its combination with chemotherapeutics has a strong anti-neoplastic effect and can induce ROS-mediated cytotoxicity at concentrations in the micromolar (μM) range, which may not be feasible with dietary interventions. Enhancing the in vivo pharmacokinetic properties of apigenin may be indispensable for its potential cancer-specific pro-oxidant therapy and may provide relevant information for clinical studies of apigenin either as a single agent or an adjuvant to chemotherapeutics.

show abstract

Protective effects of apigenin against 3-MCPD-induced renal injury in rat

Cited by 24 publications

References 44 publications

Bibliometric Analysis of Research Trends on 3-Monochloropropane-1,2-Diol Esters in Foods

Bibliometric Analysis of Research Trends on 3-Monochloropropane-1,2-Diol Esters in Foods

The role of PGC‐1α and metabolic signaling pathway in kidney injury following chronic administration with 3‐MCPD as a food processing contaminant

Reactive oxygen species: Key players in the anticancer effects of apigenin?

Contact Info

Product

Resources

About