6ʹʺ‐p‐Coumaroylspinosin protects PC12 neuronal cells from acrylamide‐induced oxidative stress and apoptosis

Abstract

6ʹʺ‐p‐coumaroylspinosin (P‐CS) is a flavonoid isolated from Ziziphi Spinosae Semen (ZSS), whereas, the antioxidative activity has not been reported. Oxidative stress is believed to be one of the main causes of neurodegenerative disorders. In this study, the antioxidative effect of P‐CS on PC12 cells was determined. The cells were treated with acrylamide (AA) in the absence or presence of P‐CS, and cell apoptosis was analyzed. Interestingly, P‐CS pretreatment of the cells could significantly prevent AA‐induced cell death, glutathione (GSH) contents decrease, and reactive oxygen species (ROS) overproduction. Further investigation of the molecular mechanism underlying the effect of P‐CS on cell apoptosis revealed that P‐CS was able to suppress the expression of Bax and Bim induced by AA and inhibit the JNKs pathway. Our findings support a role of P‐CS in preventing neuronal cell apoptosis induced by AA, suggesting its therapeutic potential for the treatment of neurodegenerative disorders as a medicinal supplement. Practical applications Oxidative stress is believed to cause damage in subcellular organelles, nucleic acids, and alteration in protein aggregation as well as disruption of the signaling cascades associated with aging and apoptosis. A small molecule, non‐poisonous natural antioxidant is needed to protect the brain from oxidative stress. Compared with western medicine, natural products carry less risk of adverse effects and are not too expensive, especially for the third‐world countries. Furthermore, ZSS could be used to produce or prepare antioxidants, such as P‐CS, which has been reported significant anti‐oxidative activity in this study.

[Retracted] Protective Effect of Triphala against Oxidative Stress‐Induced Neurotoxicity

“…), hydrogen peroxide (H 2 O 2 ), and hydroxyl radicals (OH • ) [12], of which H 2 O 2 is a culprit, destroying neurons, and thus is widely used as a stimulant of neutral cells to establish an in vitro oxidative injury model [13,14]. In addition, acrylamide, a vinyl monomer formed in high-temperature foods [15], is applied as a neurotoxin in various cell and animal models for its overproduction of ROS. For instance, acrylamide was suggested to induce cell apoptosis in human neuroblastoma SH-SY5Y cells [16] and promote neurotoxicity in the zebrafish model [17].…”

Acrylamide, acrylic acid, or 2‐acrylamido‐2‐methyl‐1‐propanesulfonic acid induced cytotoxic in Photobacterium phosphoreum, PC12, and SK‐N‐SH cells

“…In order to regulate the normal internal environment, cells are stable through a genetically spontaneous and orderly death called apoptosis 26 . It was reported that ACR exposure could activate the mitochondrial apoptotic pathway via activation of caspase 3 in PC12 cells and human neuroblastoma cells (SH‐SY5Y) 27,28 …”

“…Activation of caspase 9 was an early event in the mitochondrial involved apoptosis 5,32 . ACR has been reported that it could trigger the release of cleavage of caspase 9 and activate the mitochondrial apoptotic pathway in PC12 cells 27 . We used the activated caspase 9 antibody to determine the activated caspase 9 involved in the apoptosis pathway in PC12 and SK‐N‐SH cells treated with AA, ACR and AMPS.…”

Flavonoids: Potential Candidates for the Treatment of Neuro-Degenerative Disorders

“…Administration of 6ʹʺ-p-coumaroylspinosin (P-CS) (flavonoid isolated from Ziziphi Spinosae Semen) on PC12 neuronal cells significantly prevents acrylamide-induced cell death, decreases GSH content, and ROS overproduction. P-CS was also suppressing the expression of Bax (apoptosis regulator) and Bim (pro-apoptotic protein) induced by acrylamide and inhibits the JNKs pathway [16].…”