Polyphenols play an important role on the health-promoting properties of humans. Plants belonging to Lamiaceae family are known as rich source of phenolic compounds. The current work aimed to evaluate the phenolic compounds, antioxidant, and anti-inflammatory activity of Elsholtzia ciliata (Thunb.) Hyl. ethanolic extracts from leaf, stem, flower, and whole herb. Twelve compounds were identified in ethanolic extracts using high-performance liquid chromatography (HPLC). The HPLC analysis revealed that chlorogenic acid, rosmarinic acid, and rutin were predominant compounds in ethanolicic extracts. Using HPLC-ABTS (2,2’-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid)) post-column assay, avicularin, chlorogenic, and rosmarinic acids were identified as the predominant radical scavengers in all ethanolic extracts. All tested preparations significantly reduced the level of secretion of proinflammatory cytokines TNF-α, IL-6, and prostaglandin E2 induced by lipopolysaccharide treatment in mouse peritoneal macrophage cell culture. Stem and flower extracts were most efficient in reducing cytokine release, but leaf extract demonstrated stronger effect on prostaglandin E2 secretion. This is the first study exploring antioxidant efficiency by HPLC–ABTS post-column method and investigating anti-inflammatory activity of ethanolic extracts from E. ciliata different plant parts.

Aluminum accumulation, glutathione (GSH) and malondialdehyde (MDA) concentrations as well as catalase (CAT) and superoxide dismutase (SOD) activities were determined in erythrocytes and brain and liver homogenates of BALB/c mice treated with Al³⁺ (7.5 mg/kg/day (0.15 LD₅₀) as AlCl₃ (37.08 mg/kg/day), whereas HCl (30.41 mg/kg/day) was used as Cl⁻ control, the treatments were performed for 21 days, i.p., in the presence and absence of rosmarinic acid (0.2805 mg/kg/day (0.05 LD₅₀), 21 days, i.g.) or carvacrol (0.0405 mg/kg/day (0.05 LD₅₀), 21 days, i.g.). The treatment with AlCl₃ increased GSH concentration in erythrocytes only slightly and had no effect on brain and liver homogenates. Rosmarinic acid and carvacrol strongly increased GSH concentration in erythrocytes but decreased it in brain and liver homogenates. However, AlCl₃ treatment led to Al accumulation in mice blood, brain, and liver and induced oxidative stress, assessed based on MDA concentration in the brain and liver. Both rosmarinic acid and carvacrol were able to counteract the negative Al effect by decreasing its accumulation and protecting tissues from lipid peroxidation. AlCl₃ treatment increased CAT activity in mice brain and liver homogenates, whereas the administration of either rosmarinic acid or carvacrol alone or in combination with AlCl₃ had no significant effect on CAT activity. SOD activity remained unchanged after all the treatments in our study. We propose that natural herbal phenolic compounds rosmarinic acid and carvacrol could be used to protect brain and liver against aluminum induced oxidative stress leading to lipid peroxidation.

In recent decades, a lot of attention has been paid to Cannabis sativa L. due to its useful applications, including in fibers, oil, food for humans and animals, and therapeutics. The present study aimed to determine antioxidant activity of cannabinoids in Cannabis sativa L. in vivo, evaluating the possible antioxidative effect of Cannabis sativa L. extract (CE) on malondialdehyde (MDA) and glutathione (GSH) concentrations as well as on catalase (CAT) activity in BALB/c mice. In total, 40 mice were divided into five equal groups: the aluminum group (7.5 mg AlCl₃/kg/d (0.15 LD₅₀), the saline group, the 10% ethanol group (an appropriate amount of the solution for mouse weight), the CE group (1.6 mg CE/g/day), and the aluminum-CE group (7.5 mg AlCl₃ plus 1.6 mg CE/g/day). The results of the study showed that CE significantly decreased (by 26.81%, p < 0.05) the concentration of GSH in blood of the mice and the concentration of MDA in the brain (by 82.12%) and liver (by 53.5%) of the mice compared to the respective concentrations in the AlCl₃ group. CE significantly (p < 0.05) increased CAT activity in the brain (by 64.79%) and liver (by 72.37%) of the mice after the AlCl₃-induced prooxidant effect. The results showed the antioxidant activity of cannabidiolic acid (CBDA) in vitro. The findings in vivo indicate that Cannabis sativa L. is a good source of natural antioxidants and can be used in the management of oxidative stress.

This study was undertaken to investigate the effects of the extracts of buckwheat leaf and flower on the antioxidant status of the brain and liver tissue. The administration of buckwheat extracts (both concentrations were 10%) to mice (at the dose 10 mL/kg of body weight) for 21 days significantly decreased superoxide dismutase (SOD) activity and reduced the amount of glutathione (GSH) and malondialdehyde (MDA) in the mouse brain, while catalase (CAT) activity significantly increased. In the mouse liver, the amount of GSH and activity of SOD increased, while the CAT activity after administering buckwheat leaf and flower extracts was lower in experimental mice than in the control group. However, the administration of 10% ethanol (for 21 days) to control animals also had a significant effect on the antioxidant system in brain and liver cells. Experimental animals demonstrated rather marked changes in the activities of the antioxidant enzymes SOD and CAT in their liver and brain cells, and changes in the levels of GSH and MDA were observed when compared with the control group.

Objective. To evaluate acute toxic effect of ibogaine and noribogaine on the survival of mice and determine median lethal doses of the substances mentioned.
Material and methods. White laboratory mice were used for the experiments. Ibogaine and noribogaine were administered intragastrically to mice via a stomach tube. Control animals received the same volume of saline. The median lethal dose was calculated with the help of a standard formula.
Results. To determine the median lethal dose of ibogaine, the doses of 100, 300, 400, and 500 mg/kg were administered intragastrically to mice. The survival time of mice after the drug administration was recorded, as well as the number of survived mice in each group. Upon administration of ibogaine at a dose of 500 mg/kg, all mice in this dose group died. Three out of four mice died in the group, which received 300 mg/kg of ibogaine. No mouse deaths were observed in the group, which received 100 mg/kg of ibogaine. The determined LD50 value of ibogaine equals to 263 mg/kg of body mass. In order to determine the median lethal dose of noribogaine, the doses of 300, 500, 700, and 900 mg/kg were administered to mice intragastrically. Noribogaine given at a dose of 500 mg/kg had no impact on the mouse survival. The increase of noribogaine dose to 700 mg/kg of mouse body mass led to the death of three out of four mice in the group. Upon administration of noribogaine at a dose of 900 mg/kg, all mice in this group died. The LD50 value of noribogaine in mice determined on the basis of the number of dead mice and the size of the doses used equals to 630 mg/kg of mouse body mass. The behavior of mice was observed upon administration of ibogaine or noribogaine. Low doses of ibogaine and noribogaine had no impact on the mouse behavior. External effects (convulsions, nervous behaviour, limb paralysis) were observed only when substances were administrated at higher doses.
Conclusions. It has been determined that the median lethal dose of ibogaine and noribogaine equals to 263 mg and 630 mg/kg of mouse body mass, respectively. The toxicity of ibogaine is 2.4 times higher than that of noribogaine.