Risk assessment of in vitro cytotoxicity, antioxidant and antimicrobial activities of Mentha piperita L. essential oil.

The objective of this study was to determine the chemical composition as well as antioxidant, antibacterial, and cytotoxic properties of the essential oil of Mentha piperita L. (peppermint). Fifteen chemical constituents were identified in the essential oil, for a total of 99.99% of the compounds. The essential oil exhibited antimicrobial activity against two Gram-positive bacteria Staphylococcus aureus and Listeria monocytogenes. The minimum inhibitory concentration (MIC) of essential oil of Mentha piperita L. for Staphylococcus aureus and Listeria monocytogenes was 1.84 µg/ml, whereas the minimum bactericidal concentration (MBC) values were 3.7 and 7.43 µg/ml, respectively. The oil displayed potent antioxidant activity inhibiting up to approximately73% of 2,2'-azinothiobis (3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) radicals. In the cytotoxicity assay, the highest essential oil concentration (100 µg/ml) resulted in viability of approximately 90% human epidermal keratinocyte (HaCaT) cells. With respect to antitumor activity in C6 rat glioma cells, there was significant reduction in cell viability: 56-74% in 24 hr, and 71-77% in 48 hr. Data suggest that in presence of the essential oil of Mentha piperita L. antioxidant, antibacterial, antitumor and non-cytotoxic properties were noted.

Ketoprofen-loaded rose hip oil nanocapsules attenuate chronic inflammatory response in a pre-clinical trial in mice.

This study aimed to develop nanocapsules containing ketoprofen using rose hip oil (Keto-NC) as oil core, and to evaluate their anti-inflammatory activity in acute and chronic ear edema models in mice. Physicochemical characterization, drug release, photostability and cytotoxicity assays were performed for the developed Keto-NC formulations and compared to ketoprofen-loaded nanocapsules using medium chain triglycerides as oil core (Keto-MCT-NC). Anti-inflammatory activity of orally delivered KP (Ketoprofen-free; 10 mg.kg-1) or Keto-NC (2.5; 5; 10 mg.kg-1) was assessed in mouse acute and chronic ear edema induced by croton oil (CO). Edema histological characteristics were determined by H&E stain, and redox parameters were analyzed in blood plasma and erythrocytes. Keto-MCT-NC and Keto-NC did not exhibit differences regarding physicochemical parameters, including size diameters, polydispersity index, pH, Ketoprofen content, and encapsulation efficiency. However, Keto-NC, which contains rose hip oil as lipid core, decreased drug photodegradation under UVC radiation when compared to Keto-MCT-NC. KP or Keto-NC were not cytotoxic to keratinocyte cultures and produced equal edema inhibition in the acute protocol. Conversely, in the chronic protocol, Keto-NC was more effective in reducing edema (~60-70% on 7-9th days of treatment) when compared to KP (~40% on 8-9th days of treatment). This result was confirmed by histological analysis, which indicated reduction of edema and inflammatory infiltrate. A sub-therapeutic dose of Keto-NC (5 mg.kg-1) significantly reduced edema when compared to control. Finally, KP and Keto-NC exhibited similar effects on redox parameters, suggesting that the advantages associated with Ketoprofen nanoencapsulation did not involve oxidative stress pathways. The results showed that Keto-NC was more efficient than KP in reducing chronic inflammation. These data may be important for the development of strategies aiming treatment of chronic inflammatory diseases with fewer adverse effects.

Heparin and chondroitin sulfate inhibit adenine nucleotide hydrolysis in liver and kidney membrane enriched fractions.

The inhibition of adenine nucleotide hydrolysis by heparin and chondroitin sulfate (sulfated polysaccharides) was studied in membrane preparations from liver and kidney of adult rats. Hydrolysis was measured by the activity of NTPDase and 5'-nucleotidase. The inhibition of NTPDase by heparin was observed at three different pH values (6.0, 8.0 and 10.0). In liver, the maximal inhibition observed for ATP and ADP hydrolysis was about 80% at pH 8.0 and 70% at pH 6.0 and 10.0. Similarly to the effect observed in liver, heparin caused inhibition of ATP and ADP hydrolysis that reached a maximum of 70% in kidney (pH 8.0). Na(+), K(+) and Rb(+) changed the inhibitory potency of heparin, suggesting that its effects may be related to charge interaction. In addition to heparin, chondroitin sulfate also caused a dose-dependent inhibition in liver and kidney membranes. The maximal inhibition observed for ATP and ADP hydrolysis was about 60 and 50%, respectively. In addition, the hepatic and renal activity of 5'-nucleotidase was inhibited by heparin and chondroitin sulfate, except for kidney membranes where chondroitin sulfate did not alter AMP hydrolysis. On this basis, the findings indicate that glycosaminoglycans have a potential role as inhibitors of adenine nucleotide hydrolysis on the surface of liver and kidney cell membranes in vitro.