Background: Multidrug resistance to anticancer drugs is a major cause of chemotherapy failure in cancer patients. In efforts to find novel approaches to inhibit proliferation and induce apoptosis in lymphoma cells, we examined in both Hodgkin and non-Hodgkin lymphoma cell lines, the action of naturally occurring compound curcumin which is nontoxic and has a variety of therapeutic properties including anti-oxidant, analgesic, anti-inflammatory and antiseptic activity. Methods: Both Hodgkin and non-Hodgkin cells were pre-treated with curcumin followed by exposure to doxorubicin or vincristine and the effect on cell growth was determined. Cytotoxic effects and determination of apoptotic attributes upon curcumin treatment were analyzed using flow cytometry assays. Results: The current study demonstrates that curcumin has the ability to decrease cell viability and it is due to its capacity to decrease cell proliferation by causing cell cycle arrest in G2/M phase, and by inducing apoptotic cell death. curcumin pre-treatment followed by exposure to doxorubicin or vincristine increased apoptosis as indicated by annexin V staining. It is shown that curcumin is much more effective on lymphoma cell lines in compare to doxorubicin or vincristine. Conclusion: We have demonstrated that curcumin is an efficient inducer of apoptosis in lymphoma cell lines, meriting its further evaluation in vivo. The observed effects combined with the well established pharmacological safety of curcumin, provides rationale for the potential use of curcumin as a new therapeutic agent for patients with Hodgkin and non-Hodgkin lymphomas.

A fluorescence "off-on" probe CBF, constructed by incorporating a dioxaborine unit into a microenvironment-sensitive fluorophore, was developed for serum albumin (SA). Upon binding to SA, the dioxaborine group in CBF was hydrolyzed into β-diketonate, which triggered dramatic fluorescence enhancement (over 1000-fold) along with a remarkable blue-shift (∼100 nm). The bioimaging results suggested that more SA were taken in by cancer cells.

BackgroundSchistosomiasis mansoni is one of the most important, but often neglected, tropical diseases transmitted by snails of the genus Biomphalaria. Control of the intermediate host snail plays a crucial role in preventing the spread of schistosomiasis. However, there is only one molluscicide, niclosamide, recommended by the World Health Organization. Niclosamide has been used for several decades but is toxic to non-target organisms. Therefore, it is necessary to optimize the scaffold of niclosamide and develop novel molluscicides with enhanced potency and decreased toxicity to non-target organisms.MethodsIn this study, a candidate compound was analyzed by nuclear magnetic resonance and mass spectrometry. The molluscicidal potential against Biomphalaria species and cercaricidal potential against S. mansoni were evaluated using the immersion method. Furthermore, the preliminary mechanism was studied through cellular enzyme tests and electron microscopy.Results5-chloro-2-[(2-chloro-4-nitrophenyl)carbamoyl]phenyl-4-methoxybenzoate (salicylanilidate), a novel salicylanilide ester derivative, was derived from niclosamide. The 50% lethal concentration to B. glabrata, B. straminea and B. pfeifferi was 0.261 mg/l, 0.172 mg/l and 0.241 mg/l, respectively. The effective dose required to completely kill S. mansoni cercariae was 0.625 mg/l for salicylanilidate and 0.125 mg/l for niclosamide. However, salicylanilidate was approximately 100-fold less toxic to the fish Danio rerio than niclosamide. Furthermore, salicylanilidate reduced the enzymatic activities of nitric oxide synthase (NOS), lactate dehydrogenase (LDH) and acetylcholinesterase (AChE) in the snail, demonstrating that it could affect neurohypophysis transmission and energy metabolism. Severe swelling in the tentacle and deformation of cilia in the tentacle and mantle were observed through scanning electron microscopy. The results of transmission electron microscopy showed that salicylanilidate could damage critical organelles in hepatopancreas tissues, including degeneration of the endoplasmic reticulum and vacuolization in mitochondria. In addition, transcriptional levels of superoxide dismutase (SOD), acid phosphatase (ACP) and NOS in the hepatopancreas were significantly downregulated as shown by real-time quantitative polymerase chain reaction (RT-PCR). These results indicated that the hepatopancreas is a primary target organ of salicylanilidate.ConclusionsSalicylanilidate not only had deleterious effects on Biomphalaria species and S. mansoni cercariae but also showed very low toxicity to D. rerio, suggesting that it has broad potential applications.Electronic supplementary materialThe online version of this article (doi:10.1186/s13071-017-2313-3) contains supplementary material, which is available to authorized users.

BackgroundThe snail Biomphalaria straminea is one of the intermediate hosts of Schistosoma mansoni. Biomphalaria straminea is also an invasive species, known for its strong capability on peripheral expansion, long-distance dispersal and colonization. Using molluscicides to control snail populations is an important strategy to interrupt schistosomiasis transmission and to prevent the spread of the invasive species. In this study, a series of pyridylphenylurea derivatives were synthesized as potential molluscicides. Their impact on adult snails and egg masses was evaluated. Acute toxicity to fish of the derivatives was also examined to assess their effect on non-target organisms. The preliminary mechanisms of action of the derivatives were studied by enzyme activity assays.ResultsThe representative compounds, 1-(4-chlorophenyl)-3-(pyridin-3-yl)urea (compound 8) and 1-(4-bromophenyl)-3-(pyridin-3-yl)urea (compound 9), exhibited strong molluscicidal activity against adult snails with LD50 values of 0.50 and 0.51 mg/l and potent inhibitory effects on snail egg hatchability with IC50 values of 0.05 and 0.09 mg/l. Notably, both compounds showed good target specificity with potent molluscicidal capability observed in snails, but very low toxicity to local fishes. Furthermore, the exposure of compounds 8 and 9 significantly elevated the enzyme activities of acid phosphatase and nitric oxide synthase of the snails, while no significant change was recorded in the activities of alkaline phosphatase, acetylcholine esterase and superoxide dismutase.ConclusionThe results suggested that compounds 8 and 9 of pyridylphenylurea derivatives could be developed as promising molluscicide candidates for snail control.Electronic supplementary materialThe online version of this article (10.1186/s13071-018-2868-7) contains supplementary material, which is available to authorized users.