An Updated Review of Various Medicinal Applications of p-Co umaric Acid: From Antioxidative and Anti-Inflammatory Properties to Effects on Cell Cycle and Proliferation

Abazari, Mohammad Foad; Nasiri, Navid; Karizi, Shohreh Zare; Nejati, Fatemeh; Haghi‐Aminjan, Hamed; Norouzi, Sara; Piri, Peyman; Estakhr, Leila; Faradonbeh, Davood Rabiei; Kohandani, Mina; Daliri, Karim; Sanadgol, Nima; Askari, Hasan

doi:10.2174/1389557521666210114163024

Cited by 27 publications

(15 citation statements)

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“…The six predominant targets (TNFα, ESR1, TLR4, PTGS2, MMP9 and NOS3) have been well documented to associate with depression [24,[32][33][34][35]. Among these targets, most mediate inflammation, consistent with early reports of p-CA function [36]. Notably, this is the first time that MMP9 has been predicted as a target for p-CA.…”

Section: Discussionsupporting

confidence: 74%

P-Coumaric Acid Reverses Depression-Like Behavior and Memory Deficit Via Inhibiting AGE-RAGE-Mediated Neuroinflammation

Zhang

Xiao

et al. 2022

Cells

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Depression, a mood disorder, affects one in fifteen adults, has multiple risk factors and is associated with complicated underlying pathological mechanisms. P-coumaric acid (p-CA), a phenolic acid, is widely distributed in vegetables, fruits and mushrooms. P-CA has demonstrated a protective role against oxidative stress and inflammation in various diseases, including cardiovascular disease, diabetes and cancer. In the current study, we investigated the protection of p-CA against depression and memory impairment in a corticosterone (CORT)-induced chronic depressive mouse model. CORT administration resulted in depression-like behaviors and memory impairment. P-CA treatment alleviated CORT-induced depression-related behaviors and memory impairment. Network pharmacology predicted that p-CA had multiple targets and mediated various signaling pathways, of which inflammation-associated targets and signaling pathways are predominant. Western blotting showed CORT-induced activation of the advanced glycation end product (AGE)-receptor of AGE (RAGE) (AGE-RAGE) signaling and increased expression of the proinflammatory cytokines interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNFα) in the hippocampus, while p-CA treatment inactivated AGE-RAGE signaling and decreased the levels of IL-1β and TNFα, suggesting that protection against depression and memory impairment by p-CA is mediated by the inhibition of inflammation, mainly via the AGE-RAGE signaling pathway. Our data suggest that p-CA treatment will benefit patients with depression.

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Section: Discussionsupporting

confidence: 74%

P-Coumaric Acid Reverses Depression-Like Behavior and Memory Deficit Via Inhibiting AGE-RAGE-Mediated Neuroinflammation

Zhang

Xiao

et al. 2022

Cells

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“…P-coumaric acid treatment was also found to significantly suppress tumor growth in a xenograft model by downregulating stem cell markers and β-catenin as well as HIF-1α signaling ( Min et al, 2015 ). Further mechanistic insights demonstrated that autophagy is a novel molecular mechanism that is involved in the crosstalk between classical actions of p-coumaric acid and exerted alternative therapeutic pathways for this compound ( Abazari et al, 2021 ). Thus, we will continue to explore the anti-CSC as well as autophagic inhibition effects of p-coumaric acid on breast cancer in the future.…”

Section: Discussionmentioning

confidence: 99%

Autophagy Blockade by Ai Du Qing Formula Promotes Chemosensitivity of Breast Cancer Stem Cells Via GRP78/β-Catenin/ABCG2 Axis

et al. 2021

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Accumulating evidence suggests that the root of drug chemoresistance in breast cancer is tightly associated with subpopulations of cancer stem cells (CSCs), whose activation is largely dependent on taxol-promoting autophagy. Our pilot study identified GRP78 as a specific marker for chemoresistance potential of breast CSCs by regulating Wnt/β-catenin signaling. Ai Du Qing (ADQ) is a traditional Chinese medicine formula that has been utilized in the treatment cancer, particularly during the consolidation phase. In the present study, we investigated the regulatory effects and molecular mechanisms of ADQ in promoting autophagy-related breast cancer chemosensitivity. ADQ with taxol decreasing the cell proliferation and colony formation of breast cancer cells, which was accompanied by suppressed breast CSC ratio, limited self-renewal capability, as well as attenuated multi-differentiation. Furthermore, autophagy in ADQ-treated breast CSCs was blocked by taxol via regulation of β-catenin/ABCG2 signaling. We also validated that autophagy suppression and chemosensitizing activity of this formula was GRP78-dependent. In addition, GRP78 overexpression promoted autophagy-inducing chemoresistance in breast cancer cells by stabilizing β-catenin, while ADQ treatment downregulated GRP78, activated the Akt/GSK3β-mediated proteasome degradation of β-catenin via ubiquitination activation, and consequently attenuated the chemoresistance-promoted effect of GRP78. In addition, both mouse breast cancer xenograft and zebrafish xenotransplantation models demonstrated that ADQ inhibited mammary tumor growth, and the breast CSC subpopulation showed obscure adverse effects. Collectively, this study not only reveals the chemosensitizating mechanism of ADQ in breast CSCs, but also highlights the importance of GRP78 in mediating autophagy-promoting drug resistance via β-catenin/ABCG2 signaling.

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“…The anti-inflammatory and anti-oxidative effects of PCA have been reported in the context of various diseases, including kidney diseases ( 35 ), liver diseases ( 36 ) and osteoarthritis ( 19 ). The dosage of PCA used in different diseases ranged from 100 to 164 µg/ml ( 37 ). Huang et al ( 19 ) indicated that PCA attenuated IL-1β-induced inflammatory response and cellular senescence in chondrocytes.…”

Section: Discussionmentioning

confidence: 99%

p‑Coumaric acid suppresses reactive oxygen species‑induced senescence in nucleus pulposus cells

Sheng

Wang

et al. 2021

Exp Ther Med

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p-Coumaric acid (PCA) is a phenolic acid that is widely present in numerous plants and human diets. Studies have demonstrated the antioxidant and anti-senescence effects of PCA in different cell types. However, the anti-senescence effects of PCA in nucleus pulposus (NP) cells have remained to be determined. In the present study, reverse transcription-quantitative PCR was used to measure the gene expression of Cyclooxygenase-2 (Cox-2), inducible nitric oxide synthase (iNOS), p53, p16, aggrecan and collagen-2 in NP cells. Immunofluorescence staining was used to evaluate the protein expression of p53, p16 and collagen-2 in NP cells. In addition, cell cycle of NP cells was measured by flow cytometry. β-galactosidase staining were used to investigate the senescence of NP cells. Preliminary results indicated that PCA suppressed ROS-induced senescence in NP cells via both the p16 and p53 pathways. NP cells were pretreated with PCA at a concentration of 10 or 50 µg/ml prior to stimulation with 200 µM hydrogen peroxide (H 2 O 2 ). Pretreatment with PCA significantly inhibited H 2 O 2 -induced cell cycle arrest in a dose-dependent manner. PCA also reduced the gene expression of Cox-2, iNOS, p53 and p16 induced by H 2 O 2 . By contrast, aggrecan and collagen-2 expression in NP cells was upregulated after PCA treatment. Furthermore, PCA suppressed H 2 O 2 -induced changes in the protein expression of p16, p53 and collagen-2. H 2 O 2 stimulation of NP cells increased senescence-associated β-galactosidase (SA-β-gal) activities, while PCA treatment markedly reversed these SA-β-gal activities. Collectively, the present results indicated that PCA attenuated H 2 O 2 -induced oxidative stress and cellular senescence, suggesting a potential therapeutic utility of PCA in intervertebral disc degeneration.

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An Updated Review of Various Medicinal Applications of p-Co umaric Acid: From Antioxidative and Anti-Inflammatory Properties to Effects on Cell Cycle and Proliferation

Cited by 27 publications

References 0 publications

P-Coumaric Acid Reverses Depression-Like Behavior and Memory Deficit Via Inhibiting AGE-RAGE-Mediated Neuroinflammation

P-Coumaric Acid Reverses Depression-Like Behavior and Memory Deficit Via Inhibiting AGE-RAGE-Mediated Neuroinflammation

Autophagy Blockade by Ai Du Qing Formula Promotes Chemosensitivity of Breast Cancer Stem Cells Via GRP78/β-Catenin/ABCG2 Axis

p‑Coumaric acid suppresses reactive oxygen species‑induced senescence in nucleus pulposus cells

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