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Toxins
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Toxicity of Plant Toxins in Medical Herbs
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Toxicity of Plant Toxins in Medical Herbs

A special issue of Toxins (ISSN 2072-6651). This special issue belongs to the section "Plant Toxins".

Deadline for manuscript submissions: closed (31 October 2018) | Viewed by 20906

Special Issue Editors

Prof. Dr. Pang-Chui Shaw

E-Mail Website
Guest Editor
School of Life Sciences, The Chinese University of Hong Kong, Shatin, N.T., Hong Kong, China
Interests: structure-activity relationship of ribosome-inactivating proteins; pharmacological applications of toxins; screening of inhibitors on toxins; protein-protein interaction; toxin trafficking; toxic effects of natural products; viral proteins; quality control of herbal medicinal material
Dr. Ikhlas A. Khan

E-Mail Website
Guest Editor
National Center for Natural Products Research, The University of Mississippi, MS38677, USA

Special Issue Information

Dear Colleagues,

Herbal material is popular for maintaining health and curing diseases. Globally, there are more than 25,000 documented species of medicinal plants. Because of the great diversity of related material, improper quality control, and processing, posioning cases are frequently found. For instance, there have been misuses of Aristolochia fangchi for Stephania tetrandra in Europe, America, and Hong Kong, leading to nephropathy. There have also been poisoning cases caused by substituting Campsis grandi with a toxic herb Datura metel, and the misuse of Dysosma versipellis, which consists of a neural toxin, podophyllotoxin, for Gentiana scabra. In many cases, medicinal herbs need to be processed to reduce their poisoning components, or to convert them into useful derivatives. For example, the tubers of Aconitum carmichaelii, processed by steaming and boiling, have their toxic diester-diterpenoid alkaloids reduced and transformed, making the herb safer for clinical application.

Advanced molecular and omics technologies allow us to better-understand the underlying effects of toxins in cells and animals.

The aim of this Special Issue is to offer an overview of the current knowledge in terms of the adverse effects, mechanisms of action, and physiological responses in cells, animals, and human after encountering toxins in medicinal herbs. Review and research articles are welcome.

Prof. Dr. Pang-Chui Shaw
Dr. Ikhlas A. Khan
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a double-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Toxins is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Medicinal herbs
  • Trafficking of toxic material
  • Cellular responses
  • Functional Omics
  • Molecular biology and physiology
  • Adverse effect of toxic material
  • Detoxicification

Published Papers (4 papers)

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Research

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17 pages, 2833 KiB  
Article
Molecular Mechanisms of Apoptosis in HepaRG Cell Line Induced by Polyphyllin VI via the Fas Death Pathway and Mitochondrial-Dependent Pathway
by Yi Liu, Xiaoxv Dong, Wenping Wang, Longtai You, Xingbin Yin, Chunjing Yang, Na Sai, Xin Leng and Jian Ni
Toxins 2018, 10(5), 201; https://doi.org/10.3390/toxins10050201 - 15 May 2018
Cited by 27 | Viewed by 4432
Abstract
Polyphyllin VI, which is an active saponin, is mainly isolated from traditional medicinal plant Paris polyphylla, which causes liver damage in rats. In the present study, we aimed to explore the potential cytotoxicity of polyphyllin VI on the growth of HepaRG cells [...] Read more.
Polyphyllin VI, which is an active saponin, is mainly isolated from traditional medicinal plant Paris polyphylla, which causes liver damage in rats. In the present study, we aimed to explore the potential cytotoxicity of polyphyllin VI on the growth of HepaRG cells and to determine the molecular mechanism. The results revealed that polyphyllin VI changed cell morphology and induced apoptosis in HepaRG cells. Flow cytometric assay displayed that polyphyllin VI promoted the generation of reactive oxygen species (ROS), depolarized the mitochondrial membrane potential (MMP), and induced S phase cell cycle arrest by decreasing the expression of cyclin A2 and CDK2, while significantly increasing the expression of p21 protein. Polyphyllin VI induced the release of cytochrome c from the mitochondria to the cytosol and activated Fas, caspase-3, -8, -9, and PARP proteins. Pretreatment with NAC and Z-VAD-FMK (ROS scavenger and caspase inhibitor, respectively) on HepaRG cells increased the percentage of viable cells, which indicated that polyphyllin VI induced cell apoptosis through mitochondrial pathway by the generation of ROS and Fas death-dependent pathway. All of the effects are in dose- and time-dependent manners. Taken together, these findings emphasize the necessity of risk assessment to polyphyllin VI and offer an insight into polyphyllin VI-induced apoptosis of HepaRG cells. Full article
(This article belongs to the Special Issue Toxicity of Plant Toxins in Medical Herbs)
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11 pages, 17894 KiB  
Article
Bavachinin Induces Oxidative Damage in HepaRG Cells through p38/JNK MAPK Pathways
by Shan Wang, Min Wang, Min Wang, Yu Tian, Xiao Sun, Guibo Sun and Xiaobo Sun
Toxins 2018, 10(4), 154; https://doi.org/10.3390/toxins10040154 - 12 Apr 2018
Cited by 29 | Viewed by 4648
Abstract
Drug-induced liver injury is one of the main causes of drug non-approval and drug withdrawal by the Food and Drug Administration (FDA). Bavachinin (BVC) is a natural product derived from the fruit of the traditional Chinese herb Fructus Psoraleae (FP). There have been [...] Read more.
Drug-induced liver injury is one of the main causes of drug non-approval and drug withdrawal by the Food and Drug Administration (FDA). Bavachinin (BVC) is a natural product derived from the fruit of the traditional Chinese herb Fructus Psoraleae (FP). There have been reports of acute liver injury following the administration of FP and its related proprietary medicines. To explore BVC hepatotoxicity and its mechanisms, we used the HepaRG cell line. In our recent research, we showed that BVC induces HepaRG cell death, mainly via BVC-induced oxidative damage. The formation of ROS is closely related to the activation of the stress-activated kinases, JNK and p38, while SP600125 (SP, JNK inhibitor) and SB203580 (SB, p38 inhibitor) pretreatment inhibited the generation of ROS. On the other hand, N-acetylcysteine (NAC) pretreatment prevented the phosphorylation of p38 but not that of JNK. Taken together, these data reveal that BVC induces HepaRG cell death via ROS and the JNK/p38 signaling pathways. Full article
(This article belongs to the Special Issue Toxicity of Plant Toxins in Medical Herbs)
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Review

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18 pages, 602 KiB  
Review
Relationships between the Toxicities of Radix Aconiti Lateralis Preparata (Fuzi) and the Toxicokinetics of Its Main Diester-Diterpenoid Alkaloids
by Mengbi Yang, Xiaoyu Ji and Zhong Zuo
Toxins 2018, 10(10), 391; https://doi.org/10.3390/toxins10100391 - 26 Sep 2018
Cited by 58 | Viewed by 5826
Abstract
The processed lateral root of Aconitum carmichaelii Deb (Aconiti Radix lateralis praeparata or Fuzi) is a potent traditional herbal medicine extensively used in treatment of cardiovascular diseases, rheumatism arthritis, and bronchitis in many Asian countries. Although Fuzi has promising therapeutic effects, its toxicities [...] Read more.
The processed lateral root of Aconitum carmichaelii Deb (Aconiti Radix lateralis praeparata or Fuzi) is a potent traditional herbal medicine extensively used in treatment of cardiovascular diseases, rheumatism arthritis, and bronchitis in many Asian countries. Although Fuzi has promising therapeutic effects, its toxicities are frequently observed. Three main C19-diester-diterpenoid alkaloids (DDAs) are believed to be the principal toxins of the herb. Although toxicokinetic profiles of the toxic DDAs have already been examined in several studies, they have seldom been correlated with the toxicities of Fuzi. The current article aimed to investigate the relationship between the up-to-date toxicokinetic data of the toxic DDAs and the existing evidence of the toxic effects of Fuzi. Relationships between the cardiac toxicity and the plasma and heart concentration of DDAs in mice and rats were established. Based on our findings, clinical monitoring of the plasma concentrations of DDAs of Fuzi is recommended to prevent potential cardiac toxicities. Additionally, caution with respect to potential hepatic and renal toxicity induced by Fuzi should be exercised. In addition, further analyses focusing on the preclinical tissue distribution profile of DDAs and on the long-term toxicokinetic-toxicity correlation of DDAs are warranted for a better understanding of the toxic mechanisms and safer use of Fuzi. Full article
(This article belongs to the Special Issue Toxicity of Plant Toxins in Medical Herbs)
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15 pages, 3285 KiB  
Review
Structural and Functional Investigation and Pharmacological Mechanism of Trichosanthin, a Type 1 Ribosome-Inactivating Protein
by Wei-Wei Shi, Kam-Bo Wong and Pang-Chui Shaw
Toxins 2018, 10(8), 335; https://doi.org/10.3390/toxins10080335 - 20 Aug 2018
Cited by 16 | Viewed by 5245
Abstract
Trichosanthin (TCS) is an RNA N-glycosidase that depurinates adenine-4324 in the conserved α-sarcin/ricin loop (α-SRL) of rat 28 S ribosomal RNA (rRNA). TCS has only one chain, and is classified as type 1 ribosome-inactivating protein (RIP). Our structural studies revealed that TCS [...] Read more.
Trichosanthin (TCS) is an RNA N-glycosidase that depurinates adenine-4324 in the conserved α-sarcin/ricin loop (α-SRL) of rat 28 S ribosomal RNA (rRNA). TCS has only one chain, and is classified as type 1 ribosome-inactivating protein (RIP). Our structural studies revealed that TCS consists of two domains, with five conserved catalytic residues Tyr70, Tyr111, Glu160, Arg163 and Phe192 at the active cleft formed between them. We also found that the structural requirements of TCS to interact with the ribosomal stalk protein P2 C-terminal tail. The structural analyses suggest TCS attacks ribosomes by first binding to the C-terminal domain of ribosomal P protein. TCS exhibits a broad spectrum of biological and pharmacological activities including anti-tumor, anti-virus, and immune regulatory activities. This review summarizes an updated knowledge in the structural and functional studies and the mechanism of its multiple pharmacological effects. Full article
(This article belongs to the Special Issue Toxicity of Plant Toxins in Medical Herbs)
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