Baccharis anomala DC. extract reduces inflammation and attenuates hepatic fibrosis in vivo by decreasing NF-kB and extracellular matrix compounds.

Baccharis anomala DC. (BA) is a plant species found in the tropical regions of South America and is widely used for its hepatoprotective effects, as well as for the treatment of gastrointestinal diseases. Studies have recently reported its antioxidant and anti-inflammatory potential. BA extract can reverse the activated phenotype of hepatic stellate cells (HSC), which plays a central role in extracellular matrix (ECM) deposition in the development of liver fibrosis. Thus, this study aimed to evaluate the effects of the treatment with BA extract on liver fibrosis in a CCl4-induced liver fibrosis model in BALB/c mice. Methanolic extract was obtained from BA leaves, a gas chromatography/mass spectrometry (GC/MS) to detect the compounds present was performed, and then administered by intraperitoneal injection in Balb/C mice at a concentration of 50 and 100 mg/kg together with the administration of CCl4 for inducing liver fibrosis. After 10 weeks, blood analysis, histopathology, oxidative stress, as well as protein and gene expression in the hepatic tissue were performed. Treatment with BA extract was able to reduce profibrotic markers by reducing the expression of α-SMA and Col-1 proteins, as well as reducing the formation of free radicals and lipid peroxidation. (BA extract showed anti-inflammatory effects in the liver by suppressing NF-kB activation and reducing gene expression of signaling targets (IL-6 and iNOS). The data obtained showed that BA extract has antifibrotic and anti-inflammatory effects.

Chemical characterization and antimicrobial activity of Baccharis vulneraria Baker essential oil against strains of microorganisms that cause cutaneous infections.

Baccharis vulneraria Baker is used popularly for the treatment of skin infections. So, this study aimed investigate the antimicrobial activity and chemical characterization of the essential oil (EO) against microorganisms that cause cutaneous infections. The EO was analyzed by GC-MS. The antimicrobial test was performed using the serial microdilution method, and the antimicrobial activity was determined by the minimum inhibitory concentration against Staphylococcus aureus, Staphylococcus epidermidis, Escherichia coli, Pseudomonas aeruginosa, Candida albicans, Trichophyton interdigitale, Trichophyton rubrum, Fusarium solani and Fusarium oxysporum within the 32-0.0625 mg/mL concentration range. Were identified 31 EO compounds. Its major compounds are bicyclogermacrene, trans-cadin-1,4-diene, ß-caryophyllene, and germacrene A. EO showed antifungal action against T. rubrum and T. interdigitale (2 and 4 mg/mL MIC, respectively). The growth of C. albicans, at 4 mg/mL, decreased by 50% compared to control. The oil had no significant potential for other microorganisms at the selected concentrations.

Bezafibrate reduces the damage, activation and mechanical properties of lung fibroblast cells induced by hydrogen peroxide.

In pulmonary fibrosis, the proliferation of fibroblasts and their differentiation into myofibroblasts is often caused by tissue damage, such as oxidative damage caused by reactive oxygen species, which leads to progressive rupture and thus destruction of the alveolar architecture, resulting in cell proliferation and tissue remodeling. Bezafibrate (BZF) is an important member of the peroxisome proliferator-activated receptor (PPARs) family agonists, used in clinical practice as antihyperlipidemic. However, the antifibrotic effects of BZF are still poorly studied. The objective of this study was to evaluate the effects of BZF on pulmonary oxidative damage in lung fibroblast cells. MRC-5 cells were treated with hydrogen peroxide (H2O2) to induce oxidative stress activation and BZF treatment was administered at the same moment as H2O2 induction. The outcomes evaluated were cell proliferation and cell viability; oxidative stress markers such as reactive oxygen species (ROS), catalase (CAT) levels and thiobarbituric acid reactive substances (TBARS); col-1 and α-SMA mRNA expression and cellular elasticity through Young's modulus analysis evaluated by atomic force microscopy (AFM). The H2O2-induced oxidative damage decreased the cell viability and increased ROS levels and decreased CAT activity in MRC-5 cells. The expression of α-SMA and the cell stiffness increased in response to H2O2 treatment. Treatment with BZF decreased the MRC-5 cell proliferation, ROS levels, reestablished CAT levels, decreased the mRNA expression of type I collagen protein (col-1) and α-smooth muscle actin (α-SMA), and cellular elasticity even with H2O2 induction. Our results suggest that BZF has a potential protective effect on H2O2-induced oxidative stress. These results are based on an in vitro experiment, derived from a fetal lung cell line and may emerge as a possible new therapy for the treatment of pulmonary fibrosis.

Milk fermentation with prebiotic flour of Vasconcellea quercifolia A.St.-Hil.

Non-conventional food plants have bioactive compounds and a high nutritional value. Among these, Vasconcellea quercifolia has nutritional benefits, but it is also easy to cultivate and has a low production cost. In this study, the flour from the unripe fruit of V. quercifolia was evaluated in terms of its potential as a prebiotic for the probiotic bacteria Lactobacillus acidophilus and Bifidobacterium lactis. To do so, fermented milk samples were prepared with 2%, 3%, and 6% of flour and 8.25 log CFU/mL of each microorganism. Samples were analyzed in terms of the number of viable cells of L. acidophilus and B. lactis, as well as pH level, total solids, titratable acidity, and texture in the course of 21 days of storage at 4ºC. The obtained microbial viability revealed the in vitro symbiotic effect of flour from V. quercifolia on the probiotic strains of L. acidophilus and B. lactis, which reached 10.20 and 11.19 log CFU/mL, respectively, after 21 days of storage, showing a significant difference in cell growth of 1.7 and 2.5 log CFU/mL compared with the control. The pH level decreased from 4.8 to 4.5 after storage time, so it did not alter the conditions for the growth of bacteria. The physical and chemical parameters analyzed did not reveal significant differences (p > 0.05), which indicates product stability. Therefore, flour from the unripe fruit of V. quercifolia has a prebiotic property and can be used as a nutritional supplement for L. acidophilus and B. lactis.

Moquiniastrum polymorphum subsp. polymorphum extract inhibits the proliferation of an activated hepatic stellate cell line (GRX) by regulating the p27 pathway to generate cell cycle arrest.

ETHNOPHARMACOLOGICAL RELEVANCE: The chosen plant and its extracts have been an alternative in the treatment of several inflammatory and oxidant diseases, and is therefore a viable option for the treatment of hepatic fibrosis. AIM OF THE STUDY: This study aimed to use Moquiniastrum polymorphum subsp. polymorphum, mainly the ethanolic extract and fractions, in the treatment of hepatic fibrosis. MATERIALS AND METHODS: Extracts were prepared from dried leaves in 100% ethanol (ET) and fractionated with an increased polarity solvent (dichloromethane to methanol). The quantification of compounds in the extracts was characterized by GCMS. The decrease in cell proliferation and the cytotoxicity of the extracts were evaluated together with the mechanisms of apoptosis and autophagy. The expression of genes associated with decreased fibrosis and cell cycle control was assessed and the production of lipid droplets was quantified by Oil Red O staining. RESULTS: The experiments showed that treatment with ET and fraction 1 (F1) inhibited the expression of CDKIs (CCDN1, CDK2, CDK4 and CDK6) through an increase in p27, related to an increase in autophagic vesicles. The extract and F1 were able to decrease proliferation and revert the activated state of GRX cells to their quiescent state. CONCLUSION: Our results suggest that extracts obtained from Moquiniastrum polymorphum subsp. polymorphum have a potential therapeutic effect against liver fibrosis.

Simvastatin attenuates inflammatory process on LPS-induced acute lung injury in mice.

Acute lung injury (ALI) is a disease of high prevalence and is characterized by the excessive production of inflammatory mediators in the lungs of people sick. Inflammation is the major characteristic of ALI and studies report that inhibition of inflammatory cytokines could be an alternative treatment. Statins such as Simvastatin (SV) are known to their use for cholesterol reduction but also for inflammatory and immunoregulatory processes. In this study, we evaluated the effects of SV on LPS-induced alveolar macrophages and in ALI mice model. Our study has demonstrated the protective effects of SV on LPS-activated alveolar macrophages RAW 264.7 and LPS-induced ALI in mice. SV treatment significantly inhibited the alveolar macrophages activation by decreasing the iNOS, IL-1ß, and IL-6 gene expression in vitro and in vivo. The treatment also decreased the inflammatory cells migration and the cytokines gene expression. Our findings suggest that SV can act as an anti-inflammatory agent for acute lung injury.