Synthesis of caffeic acid sulfonamide derivatives and their protective effect against H2O2 induced oxidative damage in A549 cells

Caffeic acid phenethyl ester (CAPE), an active component of propolis, has been attracting the attention of different medical and pharmaceutical disciplines in recent years because of its antioxidant, anti-inflammatory, antiproliferative, cytotoxic, antiviral, antifungal, and antineoplastic properties. One of the most studied organs for the effects of CAPE is the kidney, particularly in the capacity of this ester to decrease the nephrotoxicity induced by several drugs and the oxidative injury after ischemia/reperfusion (I/R). In this review, we summarized and critically evaluated the current knowledge regarding the protective effect of CAPE in nephrotoxicity induced by several special medicines such as cisplatin, doxorubicin, cyclosporine, gentamycin, methotrexate, and other causes leading to oxidative renal injury, namely, I/R models and senility.

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Possible involvement of transcriptional activation of nuclear factor erythroid 2-related factor 2 (Nrf2) in the protective effect of caffeic acid on paraquat-induced oxidative damage in Drosophila melanogaster

Pesticide Biochemistry and Physiology ◽

10.1016/j.pestbp.2019.03.017 ◽

2019 ◽

Vol 157 ◽

pp. 161-168 ◽

Cited By ~ 7

Author(s):

Ricardo Gomes dos Santos Nunes ◽

Pedro Silvino Pereira ◽

Olusola Olalekan Elekofehinti ◽

Kleber Ribeiro Fidelis ◽

Cícera Simoni da Silva ◽

...

Keyword(s):

Drosophila Melanogaster ◽

Oxidative Damage ◽

Protective Effect ◽

Caffeic Acid ◽

Transcriptional Activation ◽

Related Factor ◽

Nuclear Factor

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Protective effect of caffeic acid phenethyl ester (CAPE) administration on cisplatin-induced oxidative damage to liver in rat

Cell Biochemistry and Function ◽

10.1002/cbf.1232 ◽

2006 ◽

Vol 24 (4) ◽

pp. 357-361 ◽

Cited By ~ 76

Author(s):

Mustafa Iraz ◽

Elif Ozerol ◽

Mukaddes Gulec ◽

Seda Tasdemir ◽

Nuri Idiz ◽

...

Keyword(s):

Oxidative Damage ◽

Protective Effect ◽

Caffeic Acid ◽

Caffeic Acid Phenethyl Ester

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Apigenin Protects Mouse Retina against Oxidative Damage by Regulating the Nrf2 Pathway and Autophagy

Oxidative Medicine and Cellular Longevity ◽

10.1155/2020/9420704 ◽

2020 ◽

Vol 2020 ◽

pp. 1-14 ◽

Cited By ~ 2

Author(s):

Yuanzhong Zhang ◽

Yan Yang ◽

Haitao Yu ◽

Min Li ◽

Li Hang ◽

...

Keyword(s):

Oxidative Damage ◽

Oral Bioavailability ◽

Oxidative Injury ◽

Age Related Macular Degeneration ◽

Mouse Retina ◽

Dependent Manner ◽

Nrf2 Pathway ◽

Model Mouse ◽

Dry Amd ◽

Better Than

Oxidative stress is a critical factor in the pathology of age-related macular degeneration (AMD). Apigenin (AP) is a flavonoid with an outstanding antioxidant activity. We had previously observed that AP protected APRE-19 cells against oxidative injury in vitro. However, AP has poor water and fat solubility, which determines its low oral bioavailability. In this study, we prepared the solid dispersion of apigenin (AP-SD). The solubility and dissolution of AP-SD was significantly better than that of the original drug, so the oral bioavailability in rats was better than that of the original drug. Then, the effects of AP-SD on the retina of a model mouse with dry AMD were assessed by fundus autofluorescence (FAF), optical coherence tomography (OCT), and electron microscopy; the results revealed that AP-SD alleviated retinopathy. Further research found that AP-SD promoted the nuclear translocation of Nrf2 and increased expression levels of the Nrf2 and target genes HO-1 and NQO-1. AP-SD enhanced the activities of SOD and GSH-Px and decreased the levels of ROS and MDA. Furthermore, AP-SD upregulated the expressions of p62 and LC3II in an Nrf2-dependent manner. However, these effects of AP-SD were observed only in the retina of Nrf2 WT mice, not in Nrf2 KO mice. In addition, the therapeutic effect of AP-SD was dose dependent, and AP did not work. In conclusion, AP-SD significantly enhanced the bioavailability of the original drug and reduced retinal oxidative injury in the model mouse of dry AMD in vivo. The results of the underlying mechanism showed that AP-SD upregulated the expression of antioxidant enzymes through the Nrf2 pathway and upregulated autophagy, thus inhibiting retinal oxidative damage. AP-SD may be a potential compound for the treatment of dry AMD.

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