Quercetin ameliorates oxidative stress‑induced cell apoptosis of seminal vesicles via activating Nrf2 in type 1 diabetic rats

Dong, Bingzheng; Dong, Yang; Chen, Jiangang; Wu, Zhuo‐Xun; Wu, Wei; Chen, Zhe‐Sheng; Han, Conghui

doi:10.1016/j.biopha.2022.113108

Cited by 15 publications

(13 citation statements)

References 32 publications

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“…Figures S1 and S3 ). Previous studies have shown that quercetin could direct scavenge the common small free radicals, such as HOO • , • NO and O 2 •− , then inhibit intracellular ROS accumulation [ 44 , 45 ]. In addition, many studies have reported that quercetin supplementation could effectively improve drugs, environmental toxins, and chronic diseases-induced cell or tissue damage by inhibiting the production of ROS, oxidative stress, and cell apoptosis [ 45 , 46 , 47 , 48 , 49 , 50 ].…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have shown that quercetin could direct scavenge the common small free radicals, such as HOO • , • NO and O 2 •− , then inhibit intracellular ROS accumulation [ 44 , 45 ]. In addition, many studies have reported that quercetin supplementation could effectively improve drugs, environmental toxins, and chronic diseases-induced cell or tissue damage by inhibiting the production of ROS, oxidative stress, and cell apoptosis [ 45 , 46 , 47 , 48 , 49 , 50 ]. Taken together, our results suggest that inhibiting ROS generation and increasing the activity of cellular antioxidant enzymes may contribute to quercetin’s protective impact against QCT-induced cytotoxicity in human L02 cells.…”

Section: Discussionmentioning

confidence: 99%

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Quercetin Attenuates Quinocetone-Induced Cell Apoptosis In Vitro by Activating the P38/Nrf2/HO-1 Pathway and Inhibiting the ROS/Mitochondrial Apoptotic Pathway

et al. 2022

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Quinocetone (QCT), a member of the quinoxaline 1,4-di-N-oxides (QdNOs) family, can cause genotoxicity and hepatotoxicity, however, the precise molecular mechanisms of QCT are unclear. This present study investigated the protective effect of quercetin on QCT-induced cytotoxicity and the underlying molecular mechanisms in human L02 and HepG2 cells. The results showed that quercetin treatment (at 7.5–30 μM) significantly improved QCT-induced cytotoxicity and oxidative damage in human L02 and HepG2 cells. Meanwhile, quercetin treatment at 30 μM significantly inhibited QCT-induced loss of mitochondrial membrane potential, an increase in the expression of the CytC protein and the Bax/Bcl-2 ratio, and an increase in caspases-9 and -3 activity, and finally improved cell apoptosis. Quercetin pretreatment promoted the expression of the phosphorylation of p38, Nrf2, and HO-1 proteins. Pharmacological inhibition of p38 significantly inhibited quercetin-mediated activation of the Nrf2/HO-1 pathway. Consistently, pharmacological inhibitions of the Nrf2 or p38 pathways both promoted QCT-induced cytotoxicity and partly abolished the protective effects of quercetin. In conclusion, for the first time, our results reveal that quercetin could improve QCT-induced cytotoxicity and apoptosis by activating the p38/Nrf2/HO-1 pathway and inhibiting the ROS/mitochondrial apoptotic pathway. Our study highlights that quercetin may be a promising candidate for preventing QdNOs-induced cytotoxicity in humans or animals.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Quercetin Attenuates Quinocetone-Induced Cell Apoptosis In Vitro by Activating the P38/Nrf2/HO-1 Pathway and Inhibiting the ROS/Mitochondrial Apoptotic Pathway

et al. 2022

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“…For example, the quinic acid derivatives with caffeoyl moiety have been reported to show significant DPPH radical scavenging activity ( 44 ). Quercetin could ameliorate the oxidative stress-induced apoptosis of seminal vesicle cells by activating Nrf2 (nuclear transcription factor) in type 1 diabetic rats ( 45 ). Artemisinin also could protect against cerebral ischemia and reperfusion injury via inhibiting the NF-kB (nuclear factor kappa B) pathway ( 46 ).…”

Section: Resultsmentioning

confidence: 99%

A preliminary study of the chemical composition and bioactivity of Bombax ceiba L. flower and its potential mechanism in treating type 2 diabetes mellitus using ultra-performance liquid chromatography quadrupole-time-flight mass spectrometry and network pharmacology analysis

et al. 2022

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This study aimed to preliminary investigate the phytochemistry, bioactivity, hypoglycemic potential, and mechanism of action of Bombax ceiba L. flower (BCF), a wild edible and food plant in China. By using methanol extraction and liquid-liquid extraction, the crude extract (CE) of BCF and its petroleum ether (PE), dichloromethane (DCM), ethyl acetate (EtOAc), n-butanol (n-BuOH), and aqueous (AQ) fractions were obtained, and their chemical components and biological activities were evaluated. Further high-performance liquid chromatography (HPLC) analysis was carried out to identify and quantify the active constituents of BFC and its five fractions, and the phytochemical composition of the best-performing fraction was then analyzed by ultra-performance liquid chromatography quadrupole-time-flight mass spectrometry (UPLC/Q-TOF-MS). Finally, a network pharmacology strategy based on the chemical profile of this fraction was applied to speculate its main hypoglycemic mechanism. Results revealed the excellent biological activities of BCF, especially the EtOAc fraction. In addition to the highest total flavonoid content (TFC) (367.72 μg RE/mg E) and total phenolics content (TPC) (47.97 μg GAE/mg E), EtOAc showed the strongest DPPH⋅ scavenging ability (IC50 value = 29.56 μg/mL), ABTS⋅+ scavenging ability (IC50 value = 84.60 μg/mL), and ferric reducing antioxidant power (FRAP) (889.62 μg FeSO4/mg E), which were stronger than the positive control BHT. EtOAc also exhibited the second-best α-glucosidase inhibitory capacity and second-best acetylcholinesterase (AChE) inhibitory capacity with the IC50 values of 2.85 and 3.27 mg/mL, respectively. Also, EtOAc inhibited HepG2, MCF-7, Raw264.7, and A549 cell with IC50 values of 1.08, 1.62, 0.77, and 0.87 mg/mL, which were the second or third strongest in all fractions. Additionally, HPLC analysis revealed significant differences in the compounds’ abundance between different fractions. Among them, EtOAc had the most detected compounds and the highest content. According to the results of UPLC/Q-TOF-MS, 38 compounds were identified in EtOAc, including 24 phenolic acids and 6 flavonoids. Network pharmacological analysis further confirmed 41 potential targets of EtOAc in the treatment of type 2 diabetes, and intracellular receptor signaling pathways, unsaturated fatty acid, and DNA transcription pathways were the most possible mechanisms. These findings suggested that BCF was worthwhile to be developed as an antioxidant and anti-diabetic food/drug.

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“…In another study with diabetic rats, quercetin reduced hepatotoxicity, a complication associated with diabetes [ 115 ]. Dong et al investigated the effect of quercetin in type 1 diabetic rats and their findings after a 4-month treatment indicated that quercetin ameliorated oxidative stress-induced cell apoptosis of seminal vesicles via the activation of Nrf2 [ 116 ].…”

Section: Bioactivitymentioning

confidence: 99%

Quercetin: A Molecule of Great Biochemical and Clinical Value and Its Beneficial Effect on Diabetes and Cancer

Michala

Pritsa

2022

Diseases

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Quercetin belongs to the broader category of polyphenols. It is found, in particular, among the flavonols, and along with kaempferol, myricetin and isorhamnetin, it is recognized as a foreign substance after ingestion in contrast to vitamins. Quercetin occurs mainly linked to sugars with the most common compounds being quercetin-3-O-glucoside or as an aglycone, especially in the plant population. The aim of this review is to present a recent bibliography on the mechanisms of quercetin absorption and metabolism, bioavailability, and antioxidant and the clinical effects in diabetes and cancer. The literature reports a positive effect of quercetin on oxidative stress, cancer, and the regulation of blood sugar levels. Moreover, research-administered drug dosages of up to 2000 mg per day showed mild to no symptoms of overdose. It should be noted that quercetin is no longer considered a carcinogenic substance. The daily intake of quercetin in the diet ranges 10 mg–500 mg, depending on the type of products consumed. This review highlights that quercetin is a valuable dietary antioxidant, although a specific daily recommended intake for this substance has not yet been determined and further studies are required to decide a beneficial concentration threshold.

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Quercetin ameliorates oxidative stress‑induced cell apoptosis of seminal vesicles via activating Nrf2 in type 1 diabetic rats

Cited by 15 publications

References 32 publications

Quercetin Attenuates Quinocetone-Induced Cell Apoptosis In Vitro by Activating the P38/Nrf2/HO-1 Pathway and Inhibiting the ROS/Mitochondrial Apoptotic Pathway

Quercetin Attenuates Quinocetone-Induced Cell Apoptosis In Vitro by Activating the P38/Nrf2/HO-1 Pathway and Inhibiting the ROS/Mitochondrial Apoptotic Pathway

A preliminary study of the chemical composition and bioactivity of Bombax ceiba L. flower and its potential mechanism in treating type 2 diabetes mellitus using ultra-performance liquid chromatography quadrupole-time-flight mass spectrometry and network pharmacology analysis

Quercetin: A Molecule of Great Biochemical and Clinical Value and Its Beneficial Effect on Diabetes and Cancer

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