<i>Picrasma quassioides</i> Extract Elevates the Cervical Cancer Cell Apoptosis Through ROS-Mitochondrial Axis Activated p38 MAPK Signaling Pathway

Gong, Yi-Xi; Liu, Yue; Jin, Meihua; Han, Ying‐Hao; Li, Jing; Shen, Gui‐Nan; Xie, Dan-Ping; Ren, Chen-Xi; Yu, Liyun; Lee, Dong‐Seok; Kim, Jisu; Jo, Yu-Jin; Kwon, Jeongwoo; Lee, Jaihyung; Park, Yang Ho; Kwon, Taeho; Cui, Yudong; Sun, Haiyan

doi:10.21873/invivo.11977

Cited by 17 publications

(5 citation statements)

References 34 publications

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“…Additionally, the MAPK signaling pathway, which governs cell proliferation, differentiation, apoptosis, and inflammation, has been implicated in the pathogenesis of various diseases when dysregulated (25). Activation of ERK, JNK, and p38 MAPK by ROS is known to affect cellular responses, including apoptosis (26,27). We observed marked phosphorylation of these MAPKs in response to CDDP, indicating their involvement in the apoptotic process induced by the drug in Vero cells.…”

Section: Discussionmentioning

confidence: 61%

Cisplatin Induces Kidney Cell DeathviaROS-dependent MAPK Signaling Pathways by Targeting Peroxiredoxin I and II in African Green Monkey (Chlorocebus aethiops sabaeus) Kidney Cells

ZHANG,

XIAO,

LEE

et al. 2024

In Vivo

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Background/Aim: Cisplatin [cis-diamminedichloroplatinum(II), CDDP] is a widely used and effective antitumor drug in clinical settings, notorious for its nephrotoxic side effects. This study investigated the mechanisms of CDDP-induced damage in African green monkey kidney (Vero) cells, with a focus on the role of Peroxiredoxin I (Prx I) and Peroxiredoxin II (Prx II) of the peroxiredoxin (Prx) family, which scavenge reactive oxygen species (ROS). Materials and Methods: We utilized the Vero cell line derived from African green monkey kidneys and exposed these cells to various concentrations of CDDP. Cell viability, apoptosis, ROS levels, and mitochondrial membrane potential were assessed. Results: CDDP significantly compromised Vero cell viability by elevating both cellular and mitochondrial ROS, which led to increased apoptosis. Pretreatment with the ROS scavenger Nacetyl-L-cysteine (NAC) effectively reduced CDDP-induced ROS accumulation and subsequent cell apoptosis. Furthermore, CDDP reduced Prx I and Prx II levels in a doseand time-dependent manner. The inhibition of Prx I and II exacerbated cell death, implicating their role in CDDPinduced accumulation of cellular ROS. Additionally, CDDP enhanced the phosphorylation of MAPKs (p38, ERK, and JNK) without affecting AKT. The inhibition of these pathways significantly attenuated CDDP-induced apoptosis. Conclusion: The study highlights the involvement of Prx proteins in CDDPinduced nephrotoxicity and emphasizes the central role of ROS in cell death mediation. These insights offer promising avenues 630

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Section: Discussionmentioning

confidence: 61%

Cisplatin Induces Kidney Cell DeathviaROS-dependent MAPK Signaling Pathways by Targeting Peroxiredoxin I and II in African Green Monkey (Chlorocebus aethiops sabaeus) Kidney Cells

ZHANG,

XIAO,

LEE

et al. 2024

In Vivo

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“…The p38 phosphorylation inhibitor and NAC (ROS scavenger) significantly reduced the occurrence of apoptosis compared to ERK and JNK inhibitors (Figure 4). It has been reported that P. quassioides promotes apoptosis in SiHa cervical cancer cells by activating the p38/MAPK signaling pathway, which provides an effective theoretical basis for the β-CCE (monomer of P. quassioides) inducing SiHa cell apoptosis (40). However, this study has some limitations.…”

Section: Discussionmentioning

confidence: 87%

Ethyl β-Carboline-3-Carboxylate Increases Cervical Cancer Cell Apoptosis Through ROS-p38 MAPK Signaling Pathway

Sun¹,

Xie²,

Ren³

et al. 2022

In Vivo

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Background/Aim: Ethyl β-carboline-3-carboxylate (β-CCE) is one of the effective ingredients of Picrasma quassioides (P. quassioides). As a β-carboline alkaloid, it can antagonize the pharmacological effects of benzodiazepines by regulating neurotransmitter secretion through receptors, thus affecting anxiety and physiology. However, its efficacy in cancer treatment is still unclear. Materials and Methods: We explored the effect of b-CCE on SiHa cells using MTT assay, western blot, flow cytometry, LDH release, T-AOC, SOD, and MDA assays. Results: We investigated the cytotoxicity of β-CCE in SiHa cells and verified that β-CCE could induce cell apoptosis in a time-and concentration-dependent manner. In this process, treatment with β-CCE significantly increased the levels of cytoplasmic and mitochondrial reactive oxygen species (ROS), which disturb the oxidation homeostasis by regulating the total antioxidant capacity (T-AOC), superoxide dismutase (SOD) activity, and malondialdehyde (MDA) production. Notably, the addition of N-acetylcysteine (NAC) (ROS scavenger) effectively alleviated β-CCE-induced apoptosis in SiHa cells. In addition, β-CCE might activate the p38/MAPK signaling pathway, as the pre-treatment with SB203580 (p38 inhibitor) significantly reduced β-CCEinduced apoptosis in SiHa cells. Conclusion: β-CCE has an anti-tumor activity. It activates the p38/MAPK signaling pathway by increasing intracellular ROS levels, which subsequently induce SiHa cell apoptosis. Our results provide a novel therapeutic target for treatment of cervical cancer.Cervical cancer is one of the most common female cancers with a high mortality rate worldwide (1). The main causes of cervical cancer include human papillomavirus (HPV) infection, smoking, and prolonged use of oral contraceptives. Cervical cancer has no obvious symptoms, however, as the disease progresses, abnormal vaginal bleeding (2) and vaginal discharge (3), pelvic pain, or pain during sexual intercourse are observed (4). Although cervical cancer can be effectively prevented through vaccination, it is still a growing burden for many developing and developed nations lacking effective screening and treatment methods. Hence, the development of inexpensive and effective drugs against cervical cancer is extremely important.In recent years, researchers have gradually realized the benefits of using active ingredients extracted from natural herbal medicines, which have very few side effects and are cost-effective. Ethyl β-carboline-3-carboxylate (β-CCE) is a β-carboline alkaloid extracted from P. quassioides. Studies have shown that β-carboline alkaloids have many therapeutic effects; for instance, they are used to treat mice pulmonary fibrosis (5), depression (6), bacterial infections (7), inflammatory diseases (8), and cancer (9). The anti-cancer effect of β-carboline alkaloids has been widely studied for the treatment of lung (10), liver (11), gastric (12), colon (13), and ovarian cancer (14). β-CCE is one of the most effective β-carboline alkaloids. However, , the research...

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“…However, it is worth noting that the ethanolic extracts of Picrasma quassinoides, a species of Picrasma native to Asia, showed cytotoxic effect for SiHa (cervical cancer) (Gong et al, 2020) and HepG2 G12V cells (liver cancer) (Xie et al, 2020), indicating an effect dependent on the species, soil and/or climate in which these species grow. From the adjusted curve of the data obtained for the crude extract of Pau Tenente (Figure 1), it was possible to obtain the polynomial of Equation 2.…”

Section: Crude Extractmentioning

confidence: 99%

Cytotoxicity of isolated compounds from Picrasma crenata (Vell.) Engl. in animal tumor cell (HTC)

et al. 2023

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The study aim was to evaluate the cytotoxic activity, using the MTT test [3-(4,5-Dimethilthiazol-2-yl)-2,5-diphenil tetrazolium bromide], from the crude extract of Picrasma crenata (Pau Tenente) and its isolated compounds, quassin and parain, in culture of rat liver tumor cells (HTC). The test was carried out exposing the cells for 24, 48 and 72 hours to concentrations of 5, 10, 50, 100, 200, 300, 400, 500 and 1000 μg of crude extract of Pau Tenente/mL of culture medium and 1, 5, 10, 15, 20, 40, 60, 80 and 100 μg of quassin or parain compounds/mL of culture medium. The absorbances averages results obtained showed that the crude extract did not present cytotoxicity for the HTC cells in all the concentrations and evaluated times. For quassin, the concentrations of 80 and 100 μg/mL were cytotoxic, after 72 hours of treatment. For parain, the concentrations of 1, 5, 20, 40, 60, 80 and 100 µg/mL, in 72 hours, were cytotoxic, revealing a new activity for this compound. Thus, the results demonstrate a first indication of the cytotoxic activity of compounds quassin and parain, adding an important social and economic value to them, and may have application in future research and in pharmaceutical industry.

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Picrasma quassioides Extract Elevates the Cervical Cancer Cell Apoptosis Through ROS-Mitochondrial Axis Activated p38 MAPK Signaling Pathway

Cited by 17 publications

References 34 publications

Cisplatin Induces Kidney Cell DeathviaROS-dependent MAPK Signaling Pathways by Targeting Peroxiredoxin I and II in African Green Monkey (Chlorocebus aethiops sabaeus) Kidney Cells

Cisplatin Induces Kidney Cell DeathviaROS-dependent MAPK Signaling Pathways by Targeting Peroxiredoxin I and II in African Green Monkey (Chlorocebus aethiops sabaeus) Kidney Cells

Ethyl β-Carboline-3-Carboxylate Increases Cervical Cancer Cell Apoptosis Through ROS-p38 MAPK Signaling Pathway

Cytotoxicity of isolated compounds from Picrasma crenata (Vell.) Engl. in animal tumor cell (HTC)

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