Alhagi honey polysaccharides attenuate intestinal injury and immune suppression in cyclophosphamide-induced mice

2021 ◽  
Author(s):  
Gaofeng Cai ◽  
Yu Wu ◽  
Adelijiang Wusiman ◽  
Pengfei Gu ◽  
Ningning Mao ◽  
...  
Keyword(s):  
Side Effects ◽  
Immune Suppression ◽  
Mucosal Damage ◽  
Intestinal Injury ◽  
Anti Cancer ◽  
Cancer Agent

Cyclophosphamide (Cy), extensively used as an anti-cancer agent, could cause diverse side effects such as immunosuppression and intestinal mucosal damage. Alhagi honey polysaccharides (AH), a polysaccharide isolated from Alhagi honey,...

Gastrin, Nitric Oxide Synthase and their Role in Ulceration and Distention of Stomach after Cisplatin and Taxol Treatment

1997 ◽  
Vol 3 (S2) ◽  
pp. 85-86
Author(s):  
Ying Wang ◽  
Surinder K. Aggarwal
Keyword(s):  
Side Effects ◽  
Chemotherapeutic Agent ◽  
Severe Nausea ◽  
Smooth Muscle Contractility ◽  
Anti Cancer ◽  
Gastrointestinal Side Effects ◽  
Cancer Agent ◽  
Oxide Synthase ◽  
Head Neck

Cisplatin, a potent broad spectrum anti-cancer agent, has been proven effective in the treatment of different kinds of cancer, such as bladder, lung, ovarian, head, neck, etc.. Drawbacks of this chemotherapeutic drug are its toxic side-effects, which include severe nausea, vomiting, stomach distention and peptic ulcer.Taxol is another effective chemotherapeutic agent which is usually used in conjection with cisplatin. It has demonstrated impressive activity in breast, ovarian, lung, and head and neck cancers. The toxic side-effects include nausea, vomiting, nephrotoxicity. The mechanism of these gastrointestinal side-effects are still unclear. Because of the role of NOS and gastrin on stomach smooth muscle contractility and gastroprotection, these were studied in the rats after cisplatin and taxol administration.Wistar rats(100-150 g) were injected with cisplatin(9 mg/kg) and taxol(20 mg/kg) in five divided dosages over a period of 5 days. Rats were killed one day after the last injection. Rat stomach tissues were fixed in Bouin’s solution and processed for light microscopy.

Benzoxazinoids in human diet: an anti-cancer agent?

2019 ◽  
Author(s):  
B Bhattarai ◽  
SK Steffensen ◽  
PL Gregersen ◽  
JH Jensen ◽  
KD Sørensen ◽  
...  
Keyword(s):  
Human Diet ◽  
Anti Cancer ◽  
Cancer Agent

Future Oncotargets: Targeting Overexpressed Conserved Protein Targets in Androgen Independent Prostate Cancer Cell Lines

2020 ◽  
Vol 20 (8) ◽  
pp. 1017-1027
Author(s):  
Abdul M. Baig ◽  
Zohaib Rana ◽  
Mohammad M. Mannan ◽  
Areeba Khaleeq ◽  
Fizza Nazim ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Lines ◽  
Drug Efflux ◽  
Adapter Proteins ◽  
Cancer Drugs ◽  
Protein Targets ◽  
Anti Cancer ◽  
Drug Efflux Pumps ◽  
Cancer Agent ◽  
Androgen Independent

Background: Targeting evolutionarily conserved proteins in malignant cells and the adapter proteins involved in signalling that generates from such proteins may play a cardinal role in the selection of anti-cancer drugs. Drugs targeting these proteins could be of importance in developing anti-cancer drugs. Objectives: We inferred that drugs like loperamide and promethazine that act as antagonists of proteins conserved in cancer cells like voltage-gated Calcium channels (Cav), Calmodulin (CaM) and drug efflux (ABCB1) pump may have the potential to be re-purposed as an anti-cancer agent in Prostate Cancer (PCa). Methods: Growth and cytotoxic assays were performed by selecting loperamide and promethazine to target Cav, CaM and drug efflux (ABCB1) pumps to elucidate their effects on androgen-independent PC3 and DU145 PCa cell lines. Results: We show that loperamide and promethazine in doses of 80-100μg/ml exert oncocidal effects when tested in DU145 and PC3 cell lines. Diphenhydramine, which shares its targets with promethazine, except the CaM, failed to exhibit oncocidal effects. Conclusion: Anti-cancer effects can be of significance if structural analogues of loperamide and promethazine that specifically target Cav, CaM and ABCB1 drug efflux pumps can be synthesized, or these two drugs could be re-purposed after human trials in PCa.

Nitrogen Mustards as Alkylating Agents: A Review on Chemistry, Mechanism of Action and Current USFDA Status of Drugs

2019 ◽  
Vol 19 (9) ◽  
pp. 1080-1102 ◽  
Author(s):  
Ghansham S. More ◽  
Asha B. Thomas ◽  
Sohan S. Chitlange ◽  
Rabindra K. Nanda ◽  
Rahul L. Gajbhiye
Keyword(s):  
Side Effects ◽  
Mechanism Of Action ◽  
Anticancer Agents ◽  
Nitrogen Mustard ◽  
Alkylating Agents ◽  
Cross Linking ◽  
Nitrogen Mustards ◽  
Information Leaflets ◽  
Anti Cancer ◽  
Approved Drugs

Background & Objective: :Nitrogen mustard derivatives form one of the major classes of anti-cancer agents in USFDA approved drugs list. These are polyfunctional alkylating agents which are distinguished by a unique mechanism of adduct formation with DNA involving cross-linking between guanine N-7 of one strand of DNA with the other. The generated cross-linking is irreversible and leads to cell apoptosis. Hence it is of great interest to explore this class of anticancer alkylating agents.Methods::An exhaustive list of reviews, research articles, patents, books, patient information leaflets, and orange book is presented and the contents related to nitrogen mustard anti-cancer agents have been reviewed. Attempts are made to present synthesis schemes in a simplified manner. The mechanism of action of the drugs and their side effects are also systematically elaborated.Results::This review provides a platform for understanding all aspects of such drugs right from synthesis to their mechanism of action and side effects, and lists USFDA approved ANDA players among alkylating anticancer agents in the current market.Conclusion: :Perusing this article, generic scientists will be able to access literature information in this domain easily to gain insight into the nitrogen mustard alkylating agents for further ANDA development. It will help the scientific and research community to continue their pursuit for the design of newer and novel heterocyclic alkylating agents of this class in the coming future.

Calotropis procera (Aiton) Dryand (Apocynaceae) as an anti-cancer agent against canine mammary tumor and osteosarcoma cells

2021 ◽  
Author(s):  
Ana CarolinaSilveira Rabelo ◽  
Jéssica Borghesi ◽  
Ana Claudia O. Carreira ◽  
Rafael Gonçalves Hayashi ◽  
Fernanda Bessa ◽  
...  
Keyword(s):  
Mammary Tumor ◽  
Calotropis Procera ◽  
Canine Mammary Tumor ◽  
Osteosarcoma Cells ◽  
Anti Cancer ◽  
Cancer Agent

scholarly journals Metformin induces Ferroptosis by inhibiting UFMylation of SLC7A11 in breast cancer

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Jingjing Yang ◽  
Yulu Zhou ◽  
Shuduo Xie ◽  
Ji Wang ◽  
Zhaoqing Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Treatment ◽  
Morphological Changes ◽  
Tumor Model ◽  
Independent Manner ◽  
Regulated Cell Death ◽  
Anti Cancer ◽  
Cancer Agent ◽  
Approved Drugs

Abstract Background Ferroptosis is a newly defined form of regulated cell death characterized by the iron-dependent accumulation of lipid peroxidation and is involved in various pathophysiological conditions, including cancer. Targeting ferroptosis is considered to be a novel anti-cancer strategy. The identification of FDA-approved drugs as ferroptosis inducers is proposed to be a new promising approach for cancer treatment. Despite a growing body of evidence indicating the potential efficacy of the anti-diabetic metformin as an anti-cancer agent, the exact mechanism underlying this efficacy has not yet been fully elucidated. Methods The UFMylation of SLC7A11 is detected by immunoprecipitation and the expression of UFM1 and SLC7A11 in tumor tissues was detected by immunohistochemical staining. The level of ferroptosis is determined by the level of free iron, total/lipid Ros and GSH in the cells and the morphological changes of mitochondria are observed by transmission electron microscope. The mechanism in vivo was verified by in situ implantation tumor model in nude mice. Results Metformin induces ferroptosis in an AMPK-independent manner to suppress tumor growth. Mechanistically, we demonstrate that metformin increases the intracellular Fe2+ and lipid ROS levels. Specifically, metformin reduces the protein stability of SLC7A11, which is a critical ferroptosis regulator, by inhibiting its UFMylation process. Furthermore, metformin combined with sulfasalazine, the system xc− inhibitor, can work in a synergistic manner to induce ferroptosis and inhibit the proliferation of breast cancer cells. Conclusions This study is the first to demonstrate that the ability of metformin to induce ferroptosis may be a novel mechanism underlying its anti-cancer effect. In addition, we identified SLC7A11 as a new UFMylation substrate and found that targeting the UFM1/SLC7A11 pathway could be a promising cancer treatment strategy.

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