Pharmacological effects of <i>Picrasma quassioides</i> (D. Don) Benn for inflammation, cancer and neuroprotection (Review)

Lee, Jaihyung; Gong, Yi-Xi; Jeong, Hyun-Jeong; Seo, Hoyoung; Xie, Dan-Ping; Sun, Haiyan; Kwon, Taeho

doi:10.3892/etm.2021.10792

Cited by 15 publications

(9 citation statements)

References 90 publications

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“…As an effective biological ingredient, β-CCE is widely present in P. quassioides, human urine, and the brain (28,29). The beneficial effects of β-CCE on panic disorders, anxiety, and other social behaviors were recognized through neuropsychopharmacological studies in the 1880s (30).…”

Section: Discussionmentioning

confidence: 99%

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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Section: Discussionmentioning

confidence: 99%

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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“…The bioactive compounds in GMP were quassin and picrasin B (Figure 7A) [18]. Figure 7B presents chromatograms of two standard compounds.…”

Section: Quantification Of Chemical Constituents In Gmpmentioning

confidence: 99%

“…GMP has been used to treat several symptoms, such as indigestion, gastroenteritis, pulmonary tuberculosis, and eczema [16,17]. The main components of GMP are quassinoids, triterpenoids, and alkaloids, which have a range of pharmacological effects, including anti-inflammatory, anti-cancer, and neuroprotective effects [18]. Previous studies reported that the GMP extract inhibited the allergic response in an ovalbumin-induced mouse model of asthma and suppressed the production of inflammatory mediators in RAW264.7 macrophages stimulated with lipopolysaccharide (LPS) [19,20].…”

Section: Introductionmentioning

confidence: 99%

Picrasma quassioides (D.DON) Benn. Ethanolic Extract Improves Atopic Dermatitis and Hyperactivity Disorder in DNCB-Treated BALB/c Mice

et al. 2022

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Atopic dermatitis (AD) is a chronic inflammatory skin disorder that can be associated with psychiatric disorders. Picrasma quassioides (D.Don) Benn (Gomokpi, GMP), a traditional medicinal herb, has been used to treat skin diseases, including AD. The current study examined the effects of an ethanolic extract of GMP on 2,4-dinitrochlorobenzene (DNCB)-induced AD mice. The severity of skin symptoms and behavioral changes in AD mice were evaluated. GMP alleviated the AD-like skin inflammation and hyperlocomotion activity in DNCB-treated BALB/c mice. The effects of GMP behavioral abnormalities might occur by inhibiting TNF-α production in the PFC. GMP suppressed the production of TARC (Th2 chemokine) in TI-stimulated HaCaT keratinocytes. Moreover, GMP also exerted immunosuppressive effects by reducing TNF-α production in LPS-stimulated Raw264.7 macrophages, IL-17 expression in PI-stimulated EL4 cells, and VEGF secretion in SP-stimulated HMC-1 cells. These findings suggest that GMP could be useful for treating AD by modulating inflammatory responses and comorbid behavioral changes.

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“…β-carboline alkaloids extracted from natural herbs exhibit many pharmacological effects in medical treatment that differ based on the part of the plant and species from which they have been extracted 3 . Ethyl β-carboline-3-carboxylate (β-CCE) belongs to a class of β-carboline alkaloids extracted from Picrasma quassioides 3 . This kind of alkaloid has anti-inflammatory, anti-viral 4 , anti-oxidative 5 , anti-tumour, and calming effects on brain nerves 6 .…”

Section: Introductionmentioning

confidence: 99%

“…β-carboline alkaloids extracted from natural herbs exhibit many pharmacological effects in medical treatment that differ based on the part of the plant and species from which they have been extracted [3]. Ethyl β-carboline-3-carboxylate (β-CCE) belongs to a class of β-carboline alkaloids extracted Ivyspring International Publisher from Picrasma quassioides [3].…”

Section: Introductionmentioning

confidence: 99%

Peroxiredoxin 5 protects HepG2 cells from ethyl β-carboline-3-carboxylate-induced cell death via ROS-dependent MAPK signalling pathways

Xie¹,

Gong²,

Lee³

et al. 2022

J. Cancer

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Peroxiredoxin 5 (PRDX5) is the member of Prxs family, widely reported to be involved in various types of cell death. We previously found that PRDX5 knockdown increases the susceptibility of cell death upon oxidative stress treatment. Ethyl β-carboline-3-carboxylate (β-CCE), an alkaloid extracted from Picrasma quassioides , has been reported to play a role in neuronal disease, but its anti-cancer potential on liver cancers remains unknown. Here, we studied the effect of PRDX5 on ethyl β-carboline-3-carboxylate (β-CCE)-induced apoptosis of hepatomas. High expression level of PRDX5 was deeply related with the postoperative survival of patients with liver cancer, indicating that PRDX5 may be a biomarker of live cancer processing. Moreover, PRDX5 over-expression in HepG2 cells significantly inhibited β-CCE-induced cell apoptosis and cellular ROS levels as well as mitochondrial dysfunction. Signalling pathway analysis showed that β-CCE could significantly up-regulate the ROS-dependent MAPK signalling, which were in turn boosts the mitochondria-dependent cell apoptosis. Moreover, PRDX5 over-expression could reverse the anti-cancer effects induced by β-CCE in HepG2 cells. Our findings suggest that PRDX5 has a protective role on β-CCE-induced liver cancer cell death and provides new insights for using its anti-cancer properties for liver cancer treatment.

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Pharmacological effects of Picrasma quassioides (D. Don) Benn for inflammation, cancer and neuroprotection (Review)

Cited by 15 publications

References 90 publications

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

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

Picrasma quassioides (D.DON) Benn. Ethanolic Extract Improves Atopic Dermatitis and Hyperactivity Disorder in DNCB-Treated BALB/c Mice

Peroxiredoxin 5 protects HepG2 cells from ethyl β-carboline-3-carboxylate-induced cell death via ROS-dependent MAPK signalling pathways

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