Hydroethanolic Extract of Solanum paniculatum L. Fruits Modulates ROS and Cytokine in Human Cell Lines.

Solanum paniculatum L. or popularly known as "jurubeba" is an herbal medicinal plant. A few studies have investigated its biological effects; however, research aimed at elucidating the redox balance effects from its fruits has not been reported so far. ROS interplays in various fields of medicine such as chemotherapy. Here, we evaluated antioxidant and inflammatory activities of the hydroethanolic extract of Solanum Paniculatum L. (HESPL) fruits in breast cancer cells, as well as its phytochemical profile. The antioxidant profile (carotenoids and phenolic compounds) was obtained by HPLC-DAD-UV and HPLC-APCI-MS. Cancer cell lines and human vein endothelial cells (HUVECs) were cultivated and treated with 1.87-30 µg/mL of HESPL for 24 hrs. Cytotoxicity, oxidative, and inflammation biomarkers were evaluated. The dose of 30 µg/mL of the HESPL extract presented cytotoxicity in the MCF-7 cell line. However, for MDA-MB-231, the cytotoxicity was observed in the dose of 1.87 g/mL. The 1.87 µg/mL and 3.75 µg/mL doses decreased the concentration of IL-6 in MCF-7 cells. In the MDA-MB-231 cells, the HESPL did not decrease the IL-6 concentration; however, in the doses of 15 and 30 µg/mL, an increase in this parameter was observed. The HESPL increased IL-1ß concentration in HUVECs. The ROS level in MCF-7 was elevated only at the 30 µg/ml dose. Regarding MDA-MB-231, HESPL promoted increased ROS levels at all doses tested. HUVEC showed no increase in ROS under any dose. HESPL treatment may modulate cytotoxicity, ROS, and cytokine levels due to its phytochemical profile, and it has shown an antioxidant or anti-inflammatory effect.

Fructose: Toxic effect on cardiorenal risk factors and redox state.

AIM: To investigate the effects of fructose consumption on the antioxidant capacity in heart and kidney, cardiovascular disease risk factors, and evaluation of these variables after its removal. METHODS: Male Wistar rats (n = 36) were divided into control group (n = 12): standard chow + water or F group: standard chow + fructose in drinking water (30%) for 15 weeks. After, F group was divided to continue receiving standard chow + fructose in drinking water (30%) (n = 12) or standard chow + water (Ex group, n = 12) for 9 weeks. Water, chow and caloric diaries intake, final body weight, adiposity index, plasma glucose and triacylglycerol, systolic blood pressure, and cardiac and renal hydrophilic antioxidant capacity were analyzed. RESULTS: Control and Ex groups consumed less chow and water compared to F group. Caloric intake was higher in control group. There was no difference in final body weight and adiposity index. Systolic blood pressure and cardiac and renal hydrophilic antioxidant capacity were worst in F group. CONCLUSION: Prolonged exposure to fructose induces oxidative stress, systolic blood pressure, and increase in triacylglycerol. When stopped fructose consumption, Ex group presented improvement in these variables, suggesting the toxicity effect of fructose when consumed in high amounts and prolonged exposure.

The Th17 pathway in the peripheral lung microenvironment interacts with expression of collagen V in the late state of experimental pulmonary fibrosis.

BACKGROUND: Myofibroblasts derived from fibroblasts in the pathogenesis of pulmonary fibrosis causes excessive and disordered deposition of matrix proteins, including collagen V, which can cause a Th17-mediated immune response and lead to apoptosis. However, whether the intrinsic ability of lung FBs to produce the matrix depends on their site-specific variations is not known. AIM: To investigate the link between Th17 and collagen V that maintains pulmonary remodeling in the peripheral lung microenvironment during the late stage of experimental pulmonary fibrosis. METHODS: Young male mice including wild Balb/c mice (BALB, n=10), wild C57 Black/6J mice (C57, n=10) and IL-17 receptor A knockout mice (KO, n=8), were sacrificed 21 days after treatment with bleomycin. Picrosirius red staining, immunohistochemistry for IL-17-related markers and "in situ" detection of apoptosis, immunofluorescence for collagen types I and V, primary cell cultures from tissue lung explants for RT-PCR and electron microscopy were used. RESULTS: The peripheral deposition of extracellular matrix components by myofibroblasts during the late stage is maintained in C57 mice compared with that in Balb mice and is not changed in the absence of IL-17 receptor A; however, the absence of IL-17 receptor A induces overexpression of type V collagen, amplifies the peripheral expression of IL-17 and IL-17-related cytokines and reduces peripheral lung fibroblast apoptosis. CONCLUSION: A positive feedback loop between the expression patterns of collagen V and IL-17 may coordinate the maintenance of peripheral collagen I in the absence of IL-17 receptor A in fibrosis-susceptible strains in a site-specific manner.