The present research focused on evaluating the antibacterial effect and the mechanism of action of partially purified fractions of an extract of Persea americana. Furthermore, both its antioxidant capacity and composition were evaluated. The extract was fractionated by vacuum liquid chromatography. The antimicrobial effect against Staphylococcus aureus (ATCC 6538), Escherichia coli (ATCC 11229), Pseudomonas aeruginosa (ATCC 15442), and Salmonella choleraesuis (ATCC 1070) was analyzed by microdilution and the mechanism of action by the Sytox green method. The antioxidant capacity was determined by DPPH, FRAP, and ABTS techniques and the composition by Rp-HPLC-MS. All fractions showed a concentration-dependent antibacterial effect. Fractions F3, F4, and F5 (1000 µg/mL) showed a better antibacterial effect than the extract against the bacteria mentioned. The F3 fraction showed inhibition of 95.43 ± 3.04% on S. aureus, F4 showed 93.30 ± 0.52% on E. coli, and F5 showed 88.63 ± 1.15% on S. choleraesuis and 86.46 ± 3.20% on P. aeruginosa. The most susceptible strain to the treatment with the extract was S. aureus. Therefore, in this strain, the bacterial membrane damage induced by the extract and fractions was evidenced by light fluorescence microscopy. Furthermore, the extract had better antioxidant action than each fraction. Finally, sinensitin was detected in F3 and cinnamoyl glucose, caffeoyl tartaric acid, and cyanidin 3-O-(6′′-malonyl-3′′-glucosyl-glucoside) were detected in F4; esculin and kaempferide, detected in F5, could be associated with the antibacterial and antioxidant effect.

BACKGROUND AND PURPOSE Regression of left ventricular hypertrophy by moxonidine, a centrally acting sympatholytic imidazoline compound, results from a sustained reduction of DNA synthesis and transient stimulation of DNA fragmentation. Because apoptosis of cardiomyocytes may lead to contractile dysfunction, we investigated in spontaneously hypertensive rats (SHR), time‐ and dose‐dependent effects of in vivo moxonidine treatment on cardiac structure and function as well as on the inflammatory process and signalling proteins involved in cardiac cell survival/death.EXPERIMENTAL APPROACH 12 week old SHR received moxonidine at 0, 100 and 400 µg·kg⁻¹·h⁻¹, s.c., for 1 and 4 weeks. Cardiac function was evaluated by echocardiography; plasma cytokines were measured by elisa and hearts were collected for histological assessment of fibrosis and measurement of cardiac proteins by Western blotting. Direct effects of moxonidine on cardiac cell death and underlying mechanisms were investigated in vitro by flow cytometry and Western blotting.KEY RESULTS After 4 weeks, the sub‐hypotensive dose of moxonidine (100 µg) reduced heart rate and improved global cardiac performance, reduced collagen deposition, regressed left ventricular hypertrophy, inhibited Akt and p38 MAPK phosphorylation, and attenuated circulating and cardiac cytokines. The 400 µg dose resulted in similar effects but of a greater magnitude, associated with blood pressure reduction. In vitro, moxonidine inhibited norepinephrine‐induced neonatal cardiomyocyte mortality but increased fibroblast mortality, through I₁‐receptor activation and differential effects on downstream Akt and p38 MAPK.CONCLUSIONS AND IMPLICATIONS While the antihypertensive action of centrally acting imidazoline compounds is appreciated, new cardiac‐selective I₁‐receptor agonists may confer additional benefit.

Traditionally, Equisetum hyemale has been used for wound healing. However, its mechanism of action remains to be elucidated. For this purpose, a 40% ethanolic extract of E. hyemale was prepared. Phytochemical screening revealed the presence of minerals, sterols, phenolic acids, flavonols, a lignan, and a phenylpropenoid. The extract reduced the viability of RAW 264.7 cells and skin fibroblasts at all times evaluated. On the third day of treatment, this reduction was 30–40% and 15–40%, respectively. In contrast, the extract increased the proliferation of skin fibroblasts only after 48 h. In addition, the extract increased IL-10 release and inhibited MCP-1 release. However, the extract did not affect both TGF-β1 and TNF-α released by RAW 264.7 cells. The higher release of IL-10 could be related to the up-/downregulation of inflammatory pathways mediated by the extract components associated with their bioactivity. The extract inhibited the growth of Staphylococcus aureus and Escherichia coli. Topical application of the extract accelerated wound healing in diabetic rats by increasing fibroblast collagen synthesis. These results suggest that E. hyemale extract has great potential for use in the treatment of wounds thanks to its phytochemical composition that modulates cytokine secretion, collagen synthesis, and bacterial growth.