Piperine attenuates UV-R induced cell damage in human keratinocytes via NF-kB, Bax/Bcl-2 pathway: An application for photoprotection

Verma, Ankit; Kushwaha, Hari Narayan; Srivastava, A. K.; Srivastava, Saumya; Jamal, Naseem; Srivastava, Kriti; Ray, Ratan Singh

doi:10.1016/j.jphotobiol.2017.05.018

Cited by 42 publications

(28 citation statements)

References 49 publications

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“…Piperine is a potential photochemopreventive agent. Piperine attenuates the (UV)-R induced DNA damage in human HaCaT keratinocytes through its influence on the NF-κB and Bax/Bcl-2 pathways (Verma et al, 2017 ). It is believed that piperine binds to active site of NF-κB and blocks its nuclear localization.…”

Section: Chemopreventive Mechanisms Of Piperinementioning

confidence: 99%

“…It is believed that piperine binds to active site of NF-κB and blocks its nuclear localization. Altered NF-κB activity in turn triggers suppression of apoptotic marker genes and induction of proteins involved in photoprotection (Verma et al, 2017 ). Piperine has been shown to elevate ROS formation and impair calcium homeostasis in B16F10 melanoma cells.…”

Section: Chemopreventive Mechanisms Of Piperinementioning

confidence: 99%

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Cancer Chemoprevention and Piperine: Molecular Mechanisms and Therapeutic Opportunities

Rather

Bhagat

2018

Front. Cell Dev. Biol.

138

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Cancer is a genetic disease characterized by unregulated growth and dissemination of malignantly transformed neoplastic cells. The process of cancer development goes through several stages of biochemical and genetic alterations in a target cell. Several dietary alkaloids have been found to inhibit the molecular events and signaling pathways associated with various stages of cancer development and therefore are useful in cancer chemoprevention. Cancer chemoprevention has long been recognized as an important prophylactic strategy to reduce the burden of cancer on health care system. Cancer chemoprevention assumes the use of one or more pharmacologically active agents to block, suppress, prevent, or reverse the development of invasive cancer. Piperine is an active alkaloid with an excellent spectrum of therapeutic activities such as anti-oxidant, anti-inflammatory, immunomodulatory, anti-asthmatic, anti-convulsant, anti-mutagenic, antimycobacterial, anti-amoebic, and anti-cancer activities. In this article, we made an attempt to sum up the current knowledge on piperine that supports the chemopreventive potential of this dietary phytochemical. Many mechanisms have been purported to understand the chemopreventive action of piperine. Piperine has been reported to inhibit the proliferation and survival of many types of cancer cells through its influence on activation of apoptotic signaling and inhibition of cell cycle progression. Piperine is known to affect cancer cells in variety of other ways such as influencing the redox homeostasis, inhibiting cancer stem cell (CSC) self-renewal and modulation of ER stress and autophagy. Piperine can modify activity of many enzymes and transcription factors to inhibit invasion, metastasis, and angiogenesis. Piperine is a potent inhibitor of p-glycoprotein (P-gp) and has a significant effect on the drug metabolizing enzyme (DME) system. Because of its inhibitory influence on P-gp activity, piperine can reverse multidrug resistance (MDR) in cancer cells and acts as bioavailability enhancer for many chemotherapeutic agents. In this article, we emphasize the potential of piperine as a promising cancer chemopreventive agent and the knowledge we collected in this review can be applied in the strategic design of future researches particularly human intervention trials with piperine.

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Section: Chemopreventive Mechanisms Of Piperinementioning

confidence: 99%

Section: Chemopreventive Mechanisms Of Piperinementioning

confidence: 99%

Cancer Chemoprevention and Piperine: Molecular Mechanisms and Therapeutic Opportunities

Rather

Bhagat

2018

Front. Cell Dev. Biol.

138

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“…In prostate cancer cells, inhibition of NF-KB signaling pathway suppresses cell proliferation and induces cell cycle arrest in G2/M phase associated with regulation of Bcl-2 family proteins (Bcl-2, Bax) [8]. What's more, P2Y receptors-induced proliferation of A549 cells depends on activation of NF-KB [5], which promotes transcription of downstream target genes such as Bax [7]. Therefore we detected the effect of emodin on ATP-induced activation of NF-KB and found that ATP significantly promoted translocation of NF-κB from cytoplasm to nuclear, while, emodin and suramin treatment inhibited this effect (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…. It promotes transcription of downstream target genes such as Bax [7]. Inhibition of NF-κB signaling pathway suppresses cell proliferation and induces cell cycle arrest in G2/M phase accompanied by regulation of Bcl-2 family proteins (anti-apoptotic protein Bcl-2, pro-apoptotic protein Bax) in prostate cancer cells [8].…”

Section: Introductionmentioning

confidence: 99%

Emodin Inhibits ATP-Induced Proliferation and Migration by Suppressing P2Y Receptors in Human Lung Adenocarcinoma Cells

Wang

Long

Guan

et al. 2017

Cell Physiol Biochem

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Background/Aims: Extracellular ATP performs multiple important functions via activation of P2 receptors on the cell surface. P2Y receptors play critical roles in ATP evoked response in human lung adenocarcinoma cells (A549 cells). Emodin is an anthraquinone derivative originally isolated from Chinese rhubarb, possesses anticancer properties. In this study we examined the inhibiting effects of emodin on proliferation, migration and epithelial-mesenchymal transition (EMT) by suppressing P2Y receptors-dependent Ca²⁺ increase and nuclear factor-κB (NF-KB) signaling in A549 cells. Methods: A549 cells were pretreated with emodin before stimulation with ATP for the indicated time. Then, intracellular Ca²⁺ concentration ([Ca²⁺]_i) was measured by Fluo-8/AM staining. Cell proliferation and cell cycle progression were tested by CCK8 assay and flow cytometry In addition, wound healing and western blot were performed to determine cell migration and related protein levels (Bcl-2, Bax, claudin-1, NF-κB). Results: Emodin blunted ATP/UTP-induced increase of [Ca²⁺]_i and cell proliferation concentration-dependently Meanwhile, it decreased ATP-induced cells accumulation in the S phase. Furthermore, emodin altered protein abundance of Bcl-2, Bax and claudin-1 and attenuated EMT caused by ATP. Such ATP-induced cellular reactions were also inhibited by a nonselective P2Y receptors antagonist, suramin, in a similar way to emodin. Besides, emodin could inhibit activation of NF-κB, thus suppressed ATP-induced proliferation, migration and EMT. Conclusion: Our results demonstrated that emodin inhibits ATP-induced proliferation, migration, EMT by suppressing P2Y receptors-mediated [Ca²⁺]_i increase and NF-κB signaling in A549 cells.

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“…Piperine, one of the active components of black pep-per (Piper nigrum) and long pepper (Pipper longum) (Figure 1), is commonly used as a spice in human diets, and it is also used as an effective remedy for gonorrhea, menstrual pain, tuberculosis, sleeping problems, respiratory tract infections, chronic gutrelated pain and arthritic conditions in several Asian countries and Pacific islands [12]. Piperine has been shown to possess several biological activities, including antioxidant [13,14], anti-diabetic [15], antiphotoprotective [16], anti-inflammatory [17][18][19][20][21][22][23][24] antithyroid [19], anti-platelet aggregation [25], antiobesity [26], immunomodulatory [27,28], and antitumor [29,30]. In spite of many previous studies, the mechanism by which piperine inhibits t-BHP-induced inflammation and oxidative stress has not been studied so far.…”

Section: Introductionmentioning

confidence: 99%

Anti-inflammatory and antioxidant activities of piperine on t-BHP-induced in Ac2F cells

Chung¹,

Jung²,

Kim³

et al. 2019

SDRP-JFST

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Background: In this study, to investigate whether piperine, an alkaloid from Pipper longum, could potentially exerts its effect for the suppression of inflammation and oxidative stress, we examined the modulatory effects of piperine in tert-butylhydroperoxide (t-BHP)-induced Ac2F rat liver cells. Methods: Anti-inflammatory mechanism of piperine in Ac2F cells were examined by performing western blotting. Results: The piperine exhibited remarkable reduction of intracellular reactive species (RS) levels in t-BHPand SIN-1-induced Ac2F cells. In addition, piperine inhibited t-BHP-induced activation of nuclear factor kappa B (NF-κB) by suppressing the degradation of inhibitor-κB proteins (IκBα) and translocation of p65 from the cytosol to the nucleus, further indicating piperine's inhibitory effects on nitric oxide synthase (iNOS), cyclooxyganse-2 (COX-2) expressions. As a consequence, piperine modulated through inhibition of ERK, JNK, and p38 MAPKs signal transduction pathway in cells. Moreover, piperine pretreatment also regulated the protein expression of antioxidant enzymes such as manganese-dependent superoxide dismutase (MnSOD) and catalase. Conclusion: These results indicated that piperine, a major component of black pepper might be a potential antiinflammatory agent by modulating RS-induced NF-κB activation through the MAPKs signaling pathway and possess the anti-oxidative property. Therefore piperine can be considered as a useful therapeutic and preventive approach for the treatment of inflammation and oxidative stress-related diseases.

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Piperine attenuates UV-R induced cell damage in human keratinocytes via NF-kB, Bax/Bcl-2 pathway: An application for photoprotection

Cited by 42 publications

References 49 publications

Cancer Chemoprevention and Piperine: Molecular Mechanisms and Therapeutic Opportunities

Cancer Chemoprevention and Piperine: Molecular Mechanisms and Therapeutic Opportunities

Emodin Inhibits ATP-Induced Proliferation and Migration by Suppressing P2Y Receptors in Human Lung Adenocarcinoma Cells

Anti-inflammatory and antioxidant activities of piperine on t-BHP-induced in Ac2F cells

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