Salinity Stress Affects Photosynthesis, Malondialdehyde Formation, and Proline Content in Portulaca oleracea L.

In this investigation, the effect of salt stress on Portulaca oleracea L. was monitored at salinity levels of 100 and 300 mM NaCl. At a concentration of 100 mM NaCl there was a decrease in stomatal conductance (gs) simultaneously with an increase in CO2 assimilation (A) at the beginning of salt exposure (day 3). However, the leaf water potential (ψw), the substomatal concentration of CO2 (Ci), the maximum quantum yield of photosystem II (Fv/Fm), and the proline and malondialdehyde (MDA) content remained unchanged. Exposure to 300 mM NaCl caused a decrease in gs from day 3 and a decrease in water potential, CO2 assimilation, and Fv/Fm from day 9. There was a large increase in proline content and a significantly higher MDA concentration on days 6 and 9 of salt stress compared to the control group. After 22 days of exposure to 300 mM NaCl, there was a transition from the C4 cycle to crassulacean acid metabolism (CAM), manifested by a rapid increase in substomatal CO2 concentration and negative CO2 assimilation values. These results document the tolerance of P. oleracea to a lower level of salt stress and the possibility of its use in saline localities.

Pecan pericarp extract protects against carbon tetrachloride-induced liver injury through oxidative mechanism in rats

The purpose of this study was to quantify the proanthocyanidin content of pecan (Carya illinoinensis) pericarp extract (PPE) and to assess its useful impacts against carbon tetrachloride (CCl4)-induced hepatotoxicity. Rats were randomly divided into four groups: Group 1: received intraperitoneal injection of saline solution, Group 2: was injected with PPE (25 mg/kg body weight) for 10 consecutive days, Group 3: received CCl4 (0.5 ml/kg, subcutaneous injection), Group 4: was coadministred with PPE + CCl4. The CCl4 was administered every 3 days during 10 days. Results revealed the presence of a high amount of total proanthocyanidins in the PPE (81.01 ± 0.21 mg TAE.g−1DW). CCl4 injection induced significant reductions in hepatic antioxidants but increased hepatic lipid peroxidation (LPO) as well as serum injury biomarkers. However, cotreatment with PPE significantly (P < 0.05) inverted CCl4-induced increase in plasma alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and lactate dehydrogenase activities, respectively to 74%, 77%, 60%, and 82% compared with CCl4 group. No significant toxic effects were observed following treatment with plant extract alone. PPE cotreatment also decreased significant (P < 0.05) the hepatic malondialdehyde formation (21%) and enhanced the liver catalase activity (107%) in CCl4-intoxicated rats. The histopathological examination showed inflammatory infiltration and degenerative changes in the hepatic tissue following CCl4 injection. The hepatoprotective activity of PPE against CCl4 exposure was supported by the maintenance of structural integrity of liver histopathology. In conclusion, the current study illustrated that PPE pretreatment significantly improved all examined parameters, restored the hepatic architecture and successfully alleviates oxidative damage induced by CCl4 intoxication.

Neuroprotective Effect of Anthocyanin Extract from Lycium ruthenicum Murray in Aβ1–42-induced Rat Model of AD

Alzheimer’s disease (AD) is an age-related neurodegenerative disease and is clinically characterized by cognitive impairment, memory loss, and personality disorder. Oligomers of amyloid beta-peptides (Aβ) and enhanced oxidative stress in senile plaques are prevalent pathologic hallmarks of AD. In this study, we detected the behavioral performance of Lycium ruthenicum Murray anthocyanin (LRA) -treated rats using the Morris water maze test and then investigated the effect of LRA on oxidative damage, neuronal apoptosis, and inflammatory response induced by Aβ1–42. Our results showed that LRA treatment markedly ameliorated the behavioral performance of Aβ1–42-induced rats and reduced the level of malondialdehyde, formation of protein carbonyl, and 8-hydroxy-2’-deoxygua-nosine. Furthermore, LRA also inhibited activated astrocytes and neuroinflammation via suppression of glial fibrillary acidic protein and tumor necrosis factor-alpha in the hippocampus of Aβ1–42-treated rat brain. These data suggest that LRA could be a potential anti-oxidant and anti-neuroinflammatory agent for the treatment of AD.

Antioxidant, Cytotoxic, and Toxic Activities of Propolis from Two Native Bees in Brazil:Scaptotrigona depilisandMelipona quadrifasciata anthidioides

Propolis is a natural mixture of compounds produced by various bee species, including stingless bees. This compound has been shown to exhibit antioxidant, antiproliferative, and antitumor activities. The present study aimed to determine the chemical constituents as well as the antioxidant, cytotoxic, and toxic activities of ethanol extracts of propolis obtained from the stingless beesScaptotrigona depilisandMelipona quadrifasciata anthidioides, which are found in Brazil. Phytosterols, terpenes, phenolic compounds, and tocopherol were identified in the ethanol extracts of propolis (EEPs) in different concentrations. The compounds stigmasterol, taraxasterol, vanilic acid, caffeic acid, quercetin, luteolin, and apigenin were found only in EEP-M. The EEPs were able to scavenge the free radicals 2,2-diphenyl-1-picrylhydrazyl and 2,2′-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) and protected human erythrocytes against lipid peroxidation, with the latter effect being demonstrated by their antihemolytic activity and inhibition of malondialdehyde formation. The EEPs showed cytotoxic activity against erythroleukemic cells and necrosis was the main mechanism of death observed. In addition, the concentrations at which the EEPs were cytotoxic were not toxic againstCaenorhabditis elegans. In this context, it is concluded that EEP-S and EEP-M show antioxidant and cytotoxic activities and are promising bioactive mixtures for the control of diseases associated with oxidative stress and tumor cell proliferation.