Isatin (indole-2,3-dione) is an endogenous regulator, exhibiting various behavioral, biological, and pharmacological activities. Synthesis of isatin includes several crucial stages: cleavage of the tryptophan side chain and subsequent oxidation of the indole nucleus. Although these stages require concerted action of bacterial and host enzymes, there are two pathways of isatin formation: the host and bacterial pathways. Isatin acts as a neuroprotector in different experimental models of neurodegeneration. Its effects are realized via up- and downregulation of isatin-responsive genes and via interaction with numerous isatin-binding proteins identified in the brain. The effect of isatin on protein-protein interactions in the brain may be important for realization of weak inhibition of multiple receptor targets.

/pdf/tryptophan-metabolites-as-mediators-of-microbiota-gut-brain-u687lzf4.pdf

Tryptophan Metabolites as Mediators of Microbiota-Gut-Brain Communication: Focus on Isatin

BACKGROUND
Cancer is a disease characterized by the abnormal multiplication of cells and is the second leading cause of death in the world. The search for new effective and safe anticancer compounds is ongoing due to factors such as low selectivity, high toxicity, and multidrug resistance. Thus, heterocyclic compounds derived from isatin, thiazole and phthalimide that have achieved promising in vitro anticancer activity have been tested in vivo and in clinical trials.


OBJECTIVE
This review focused on the compilation of promising data from thiazole, isatin, and phthalimide derivatives, reported in the literature between 2015 and 2022, with in vivo anticancer activity and clinical trials.


METHOD
A bibliographic search was carried out in the PUBMED, MEDLINE, ELSEVIER, and CAPES PERIODIC databases, selecting relevant works for each pharmacophoric group with in vivo antitumor activity in the last 6 years.


RESULTS
In our study, 68 articles that fit the scope were selected and critically analyzed. These articles were organized considering the type of antitumor activity and their year of publication. Some compounds reported here demonstrated potent antitumor activity against several tumor types.


CONCLUSION
This review allowed us to highlight works that reported promising structures for the treatment of various cancer types and also demonstrated that the privileged structures thiazole, isatin and phthalimide are important in the design of new syntheses and molecular optimization of compounds with antitumor activity.

Thiazole, isatin and phthalimide derivatives tested in vivo against cancer models: a literature review of the last six years.

Plant coumarins are important components of the human diet and a number of them are considered to possess chemo-preventive and therapeutic properties against cancer. Scopoletin, a natural coumarin component has been shown to inhibit the growth of many cancer cells. In this study, the cytotoxic activity of scopoletin was studied against human neuroblastoma cells SH-SY5Y. The activity of scopoletin was evaluated by Sulphorhodamine B (SRB) assay and xCELLigence system. It was demonstrated that scopoletin reduced human SH-SY5Y neuroblastoma cell viability. Scopoletin inhibited the growth of the cell line and the IC50 values were 91.82 and 79.19 μM for 48-h and 72-h, respectively. The findings from this study demonstrated that the growth inhibitory and cytotoxic effects of scopoletin on SH-SY5Y cells may prove essential in the development of novel treatment regimens for neuroblastoma cancer.

Sh-sy5y nöroblastoma hücreleri̇nde skopoleti̇n nörotoksi̇si̇tesi̇ne bağli empedans deği̇şi̇kli̇kleri̇ni̇n gerçek zamanli anali̇zi̇

Bitki kumarinleri, insan diyetinin önemli bileşenleridir ve birçoğunun kansere karşı koruyucu ve tedavi edici özelliklere sahip olduğu bilinmektedir. Doğal bir kumarin bileşeni olan skopoletinin birçok kanser hücresinin büyümesini engellediği gösterilmiştir. Bu çalışmada, insan nöroblastom hücreleri SHSY5Y'ye karşı skopoletinin sitotoksik aktivitesi incelendi. Scopoletin aktivitesi, Sulphorhodamine B (SRB) testi ve xCELLigence sistemi ile değerlendirildi. Skopoletinin insan SHSY5Y nöroblastom hücre canlılığını azalttığı gösterildi. Scopoletin hücre büyümesini inhibe etti ve IC50 değerleri 48 ve 72 saat için sırasıyla 91,82 ve 79,19 µM’dir. Bu çalışmadan elde edilen bulgular, skopoletinin SHSY5Y hücreleri üzerindeki büyüme önleyici ve sitotoksik etkilerinin, nöroblastom kanseri için yeni tedavi rejimlerinin geliştirilmesinde önemli olabileceğini kanıtladı.

/pdf/shsy5y-noroblastoma-hucrelerinde-scopoletin-25vwj6eh.pdf

SHSY5Y Nöroblastoma Hücrelerinde Scopoletin Nörotoksisitesine Bağlı Empedans Değişikliklerinin Gerçek Zamanlı Analizi

Abstract Amyloid-beta (Aβ) aggregates deposition at extra neuronal sites induces neurotoxicity and major hallmarks of Alzheimer’s disease (AD). To reduce the Aβ fibril toxicity, multi-functional polyamidoamine (PAMAM) dendrimer was conjugated with tocopheryl polyethylene glycol succinate-1000 (TPGS) which acts as a carrier matrix for the delivery of neuroprotective molecule piperine (PIP). This PIP-TPGS-PAMAM dendrimer was fabricated to mitigate the Aβ1–42 fibril toxicity on SHSY5Y cells. TPGS-PAMAM was fabricated through carbodiimide coupling reaction, and PIP was encapsulated in dendrimer through solvent injection method to prepare PIP-TPGS-PAMAM. Antioxidant assay of PIP-TPGS-PAMAM showed 90.18% inhibition of 1, 1-diphenyl-2-picrylhydrazyl (DPPH) free radicals compared to free PIP, which was 28.27%. The SHSY5Y cells showed 37.25% for negative control group and 82.55% cell viability for PIP-TPGS-PAMAM treated group against Aβ1–42 toxicity. PIP-TPGS-PAMAM reduced the ROS activity to 15.21% and 48.5% for free PIP treated in cell group. Similarly, extent of Aβ1-42-induced apoptosis also reduced significantly from 38.2% to 12.36% in PIP-TPGS-PAMAM treated group. In addition, PIP-TPGS-PAMAM also disaggregated the Aβ1–42 fibril in SHSY5Y cells. Our findings suggested that PIP-TPGS-PAMAM showed mitigation of Aβ1-42-induced toxicity in neuronal cells, which can offer excellent prospect of neuroprotection and AD therapy.

https://figshare.com/articles/journal_contribution/Formulation_development_of_tocopherol_polyethylene_glycol_nanoengineered_polyamidoamine_dendrimer_for_neuroprotection_and_treatment_of_Alzheimer_disease/19609414/1/files/34830724.pdf

Formulation development of tocopherol polyethylene glycol nanoengineered polyamidoamine dendrimer for neuroprotection and treatment of Alzheimer disease

Indoline‑2,3‑dione or indole‑1H‑2,3‑dione, commonly known as isatin, is found in plants of genus Isatin and in Couropita guianancis aubl, and inhibits tumor cell proliferation through its antioxidant effects. The present study analyzed the effect of isatin on the malignant phenotype of neuroblastoma cells, and reported that isatin significantly inhibited neuroblastoma cell proliferation, invasion and migration in vitro in a dose‑dependent manner, and distant metastasis in tumor‑bearing mice. Mechanistically, isatin inhibited lysine‑specific histone demethylase (LSD)1 and reversed the blockade on p53, thereby activating the apoptotic pathway. The inhibitory effect of isatin on LSD1 may be mediated via direct binding and molecular docking or indirectly through the TGFβ/ERK/NF‑κB signaling pathway. Isatin also alleviated the renal and hepatic toxicity of cyclophosphamide in the tumor‑bearing mice, indicating its potential as a candidate drug as well as an adjuvant for treating metastatic neuroblastoma.

Isatin inhibits the invasion and metastasis of SH‑SY5Y neuroblastoma cells in vitro and in vivo.


 Neuroblastoma (NB) is common in the pediatric tumors with low cure rate and high mortality, drug resistance makes chemotherapy more difficult, it threaten to children's health seriously. 1H-indole-2, 3-dione (isatin) is a second-hand of derivative of anticarcinogen indirubin which had been shown to be a monoamine oxidase inhibitor and have antitumor activity, in this study, we explained that SH-SY5Y cells was add to isatin at a dose-dependent level ranging from 50 to 200 µmol/L were capable of inhibiting tumor cell growth, included triggering apoptosis and inhibiting proliferation, invasion and metastasis, and assess ed the potential anticancer capability of isatin on the induction of autophagy. The experimental result showed that cell SH-SY5Y disposed with isatin could induce autophagy effectively, at the same time, it also help suppress the growth of tumor cells. Furthermore , the article indicated that the induction of autophagy of isatin-mediated occurred in inhibition- lysine-specific demethylase 1(LSD1) and sestrin2 (SESN2) - dependent manner. Furthermore, we identified that SH-SY5Y cells after treating with isatin induced SESN2 expression via a mTOR-dependent signal pathway, which mechanism is that isatin inhibit LSD1-enzyme activation and combine the promoter regions of SESN2, so that given rise to a significant transcriptional induction of SESN2. In addition , western blot analysis indicated that SH-SY5Y cells with isatin-exposed can regulated activity of LC-3, Beclin1 and p62 which are correlated with autophagy. Collectively, all the results from this study illistrated that adding to isatin could occur to induce autophagy and restrain NB cell SH-SY5Y growth through mTOR-dependent transcriptional induction of SESN2, this supplied a new mechanism for understanding the anti-tumor ability of isatin on NB. Taken together, this paper demonstrate that isatin is a promising candidate for treating NB.

/pdf/isatin-inhibits-lsd1-regulated-autophagy-through-sesn2-mtor-5869z9rj3q.pdf

Isatin inhibits LSD1 regulated autophagy through SESN2-mTOR signaling pathway in neuroblastoma

Handle everyday research tasks with reliable, citation-backed results

Your personal Research Agent to handle research tasks with citation-backed results

Popular Tasks used by Researchers

How can I help with your research?

Meet SciSpace

Get more enhanced response by uploading the PDFs you want me to reference.

No relevant PDFs in your library

SciSpace is the AI research assistant for academics. Run systematic literature reviews on 280M+ papers, and write papers with cited sources. Trusted by 1M+ students, PhDs & researchers.

SciSpace | AI for Research

Analyze PDFs

Code & Manuscripts

Funding & Grants

Literature & Patents

Medical & Clinical Data

Systematic Review

Visualize & Present

Web & Data

Build a Google Scholar-like website for your research.

Build a website

Create charts and images for your research

Create a Chart

Write a paper for submission to a journal

Draft a manuscript

Patent Search

Design eye-catching scientific posters in minutes.

Scientific Poster Generation

Systematic Literature Review

One task is running at the moment. Your messages will be shown right after.

Drag and drop or click here to browse

Loved by <highlight>1 million+</highlight> researchers

Extract a list of specific topics and their sources from unstructured text

Topics

Compare and analyze relevant papers that matches with your search

Papers

Get insights from PDFs and bookmarked papers from your library

My library

Recent searches

Try searching for:

Catch AI-generated content in scholarly and non-scholarly content

{ai} Detector

Ai Writer

Get PDF Summaries, highlighted text explanations 

Chat with PDF

Effortlessly create in-text citations and bibliographies in APA and 2,500 other formats

Citation generator

Get explanations, summaries, and answers on academic papers

Ease up your research workflow with {scispace}'s cohort of exciting AI tools

Elevate your academic writing skills and convey your ideas the way you want

Paraphraser

Explore our range of reading and writing tools

Your file is being prepared and should be ready in a few minutes. If it's a large file, it might take a bit longer. You can close this window, and we'll email you the file when it's done.

You have reached a maximum limit of <strong>{limit}</strong> columns in the table. Remove at least <strong>1</strong> column to add or create another one.

Jun Wang

Author Tools

Chat about Author

Papers

Isatin inhibits the invasion and metastasis of SH‑SY5Y neuroblastoma cells in vitro and in vivo.

Isatin inhibits LSD1 regulated autophagy through SESN2-mTOR signaling pathway in neuroblastoma