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Phyllanthus niruri L. belongs to the Euphorbiaceae, and is known by the common name of 'stonebreaker' in Brazil. Some species within the Phyllanthus genus are widely used in traditional medicine to counteract different types of anti-inflammatory diseases., Objectives: In this study, the preventive intestinal anti-inflammatory activity of spray-dried extract of P. niruri (SDEPn) was tested in the model of acetic acid (10%)-induced ulcerative colitis in the rat., Methods: Colitis animals were given orally at doses 25, 100 and 200 mg/kg. Colons tissue was analysed by macroscopic score, by histopathology score, by the immunohistochemical examination of tumour necrosis factor alpha, p53 and interferon gamma; by spectroscopic ultraviolet-visible spectrophotometry (UV/VIS) analysis of the levels of myeloperoxidase, malonaldehyde and total glutathione., Key Findings/result: Pretreatment of the extract to colitic rats significantly attenuated colonic macroscopic damage induced by acetic acid (P < 0.01). Spray-dried extract of P. niruri prevented glutathione depletion (P < 0.001) and malondialdehyde levels (P < 0.05) declined. Spray-dried extract of P. niruri significantly reduced microscopic damage to tissues, such as leukocyte infiltration accompanied by a significant reduction in myeloperoxidase activity (P < 0.5). Immunohistochemistry revealed a decline in the TNF-α, IFN-γ and p53 protein (P < 0.05)., Conclusion: Spray-dried extract of P. niruri has a beneficial effect in the acute phase of acetic acid-induced colitis in the rat, which is probably related to its antioxidant properties., (© 2015 Royal Pharmaceutical Society.)

The ability to induce apoptosis is an important marker for cytotoxic antitumor agents. Some natural compounds have been shown to modulate apoptosis pathways that are frequently blocked in human cancers, and therefore, these compounds provide novel opportunities for cancer drug development. Phyllanthus, a plant genus of the family Euphorbiaceae, exhibits multiple pharmacological actions. Of these, Phyllanthus niruri extracts exhibit significant antitumor activity, which is consistent with the traditional medicinal use of this plant. To examine the apoptotic effects of a spray-dried extract of P. niruri (SDEPN), human hepatocellular carcinoma cells (HepG2, Huh-7), colorectal carcinoma cells (Ht29) and keratinocytes (HaCaT) were exposed to the extract for 4, 8 and 24 h. Flow cytometry and caspase-3 immunostaining were used to detect apoptosis, while analysis of variance was applied to identify significant differences between groups (P < 0.05). At all timepoints, the SDEPN induced significantly different cytotoxic effects for HepG2 and Huh-7 cells compared with control cells (P < 0.001). In contrast, the SDEPN had a protective effect on HaCaT cells compared with control cells at all timepoints (P < 0.001). In caspase-3 assays, activation was detected after cell death was induced in Huh-7 and HepG2 cancer cells by the SDEPN. In combination, these results indicate that the SDEPN is selectively toxic towards cancer cell lines, yet is protective towards normal cells.

Aim: To investigate the cytotoxic effects of spray-dried extracts of Phyllanthus niruri in combination with cisplatin on two cancer cell lines., Methods: Colorectal carcinoma (HT29) and human hepatocellular carcinoma (HepG2) cells were treated with spray-dried extracts of Phyllanthus niruri (SDEPN) either alone or in combination with cisplatin at different concentrations (0.5 mg/mL and 1 mg/mL) for 4 h and 24 h. To verify and quantify cancer cells treated with these products as well as identify the cell cycle stage and cell viability, we stained the cells with propidium iodide and assessed them by flow cytometry. The percentage of cells in different cell cycle phases was quantified and data were expressed as histograms. Significant differences between groups were determined using analysis of variance and Bonferroni's test, as indicated. A value of P < 0.05 was considered to be statistically significant., Results: SDEPN had significantly different cytotoxic effects on HT29 (2.81 ± 0.11 vs 3.51 ± 1.13, P > 0.05) and HepG2 (5.07 ± 0.3 vs 15.9 ± 1.04, P < 0.001) cells when compared to control cells for 4 h. SDEPN also had significantly different cytotoxic effects on HT29 (1.91 ± 0.57 vs 4.53 ± 1.22, P > 0.05) and HepG2 (14.56 ± 1.6 vs 35.67 ± 3.94, P < 0.001) cells when compared to control cells for 24 h. Both cell lines were killed by cisplatin in a dose-dependent manner compared to control cells (HepG2 cells for 4 h: 10.78 ± 1.58 vs 53.89 ± 1.53, P < 0.001; 24 h: 8.9 ± 1.43 vs 62.78 ± 1.87, P < 0.001 and HT29 cells for 4 h: 9.52 ± 0.913 vs 49.86 ± 2.89, P < 0.001; 24 h: 11.78 ± 1.05 vs 53.34 ± 2.65, P < 0.001). In HT29 cells, pretreatment with SDEPN and subsequent treatment with cisplatin resulted in a greater number of cells being killed (12.78 ± 1.01 vs 93.76 ± 1.6, P < 0.001). HepG2 cells showed significant cell killing with treatment with SDEPN when combined with cisplatin (12.87 ± 2.78 vs 78.8 ± 3.02, P < 0.001)., Conclusion: SDEPN is selectively toxic against two cancer cell lines. Moreover, SDEPN in combination with cisplatin induces a synergistic increase in the cell death of both HT29 and HepG2 cells.