Group items tagged

the effect of a very low dose of LA (0.1 mg/kg) was potentiated by the same dose of pentoxifylline (PTX), a known TNF-alpha inhibitor. L

rich in triterpenes

Carrageenan-induced mice paw edema

LA (10, 25 and 50 mg/kg, i.p.) reduced both phases of the formalin test, and the results were significant at the two higher doses. However, the effects were mainly on the 2nd phase with 61% inhibition, whereas the 1st phase was inhibited by 41% at the LA dose of 50 mg/kg, i.p. The naloxone pretreatment completely reversed the LA effect, in the 1st and 2nd phases, indicating the participation of the opioid system in LA antinociceptive and anti-inflammatory actions.

On the other hand, while no significant enzyme release was observed with LA at the concentrations of 1, 10 and 25 μg/mL, a small but significant LDH release (around 2 times) was detected with the higher LA concentration (50 μg/mL), probably related to the presence of 0.2% Tween 80.

The results show that LA at the concentrations of 50, 100 and 200 μg/mL presents no radical scavenging capacity. On the contrary, vitamin E used as the reference drug significantly decreased the absorbance value, as related to controls

In the carrageenan-treated groups pretreated with LA (50 mg/kg, i.p.) or indomethacin (10 mg/kg, i.p.), there were significant reductions of iNOS expressing cells.

Lupeol is found in several other species and its antinociceptive and anti-inflammatory activities have been already demonstrated [24–28]. It is accepted that the anti-inflammatory property of lupeol often accompany its immune modulatory and anti-tumor action

lupeol acetate presents an anti-inflammatory activity by regulating TNF-alpha and IL-2 specific mRNA, besides upregulating the synthesis of IL-10 mRNA [31].

In the present work, we showed that lupeol acetate (LA, 93.2% purity) isolated from the H. drasticus latex presented a potent anti-inflammatory action, in several models of inflammation in mice

These authors concluded that lupeol possessed an anti-inflammatory activity which is probably related to its ability to prevent the production of pro-inflammatory mediators, such as TNF-α and IL-1β.

In this line of research, novel therapies aim to target apoptosis via mitochondria, using molecules that mimic BH3 proteins and disrupt the interactions of pro-apoptotic and anti-apoptotic proteins.

Therefore, the mechanisms by which mushroom extracts or isolated compounds induce mitochondrial-related apoptosis pathways are diverse and may be related with specific bioactive compounds. Modulation of pathways crucial for cell survival and alterations in lipid homeostasis seem to be related with the pro-apoptotic effects observed in HCC cell lines and in in-vivo xenograft models.

To sum up, mitochondria play a central role in the pathophysiology and progression of NAFLD as well as in the development of HCC, which can be a late-stage consequence of NASH. Hepatic mitochondria undergo bioenergetic remodelling to face the metabolic burden imposed by the increased FFAs load secondary to systemic IR. In turn, a decompensation of these processes may result in ROS formation and mitochondrial dysfunction, contributing to the development of NASH. Lastly, hepatic mitochondria also seem to be involved in anti-apoptotic oncogenic processes driving HCC. Targeting mitochondrial dysfunction is thus a promising approach for the treatment of the NAFLD continuum. The following section describes some of the in-vitro and in-vivo studies on the beneficial effects of mushroom-enriched diets or mushroom-derived compounds/extracts (Box 2) in preventing/reverting such liver damage.