Bioassay-guided separation of young leaves extracts of Syzygium antisepticum (Blume) Merr. & L.M. Perry led to the isolation of four triterpenoids (betulinic acid, ursolic acid, jacoumaric acid, corosolic acid) and one sterol glucoside (daucosterol) from the ethyl acetate extract, and three polyphenols (gallic acid, myricitrin, and quercitrin) from the methanol (MeOH) extract. The MeOH extract of S. antisepticum and some isolated compounds, ursolic acid and gallic acid potentially exhibited acetylcholinesterase activity evaluated by Ellman’s method. The MeOH extract and its isolated compounds, gallic acid, myricitrin, and quercitrin, also strongly elicited DPPH radical scavenging activity. In HEK-293 cells, the MeOH extract possessed cellular antioxidant effects by attenuating hydrogen peroxide (H₂O₂)-induced ROS production and increasing catalase, glutathione peroxidase-1 (GPx-1), and glutathione reductase (GRe). Furthermore, myricitrin and quercitrin also suppressed ROS production induced by H₂O₂ and induced GPx-1 and catalase production in HEK-293 cells. These results indicated that the young leaves of S. antisepticum are the potential sources of antioxidant and anticholinesterase agents. Consequently, S. antisepticum leaves are one of indigenous vegetables which advantage to promote the health and prevent diseases related to oxidative stress.

Organic solvents are commonly used to extract lutein. However, they are toxic and are not environmental-friendly. There are only a few reports on the quantification of lutein. Therefore, this study aimed to determine a suitable extraction method by which to obtain lutein from marigold flower (Tagetes erecta L.), using coconut oil to evaluate the cytotoxicity of extract in ARPE-19 cells, to optimize the encapsulation process for the development of microencapsulated marigold flower extract, and to develop the method for analysis of lutein by using UHPLC-Q-Orbitrap-HRMS. Coconut oil was used for the extraction of marigold flowers with two different extraction methods: ultrasonication and microwave-assisted extraction. The UHPLC-Q-Orbitrap-HRMS condition for the analysis of lutein was successfully developed and validated. Marigold flower extract obtained using the microwave method had the highest lutein content of 27.22 ± 1.17 mg/g. A cytotoxicity study revealed that 16 µM of lutein from marigold extract was non-toxic to ARPE-19 cells. For the development of microencapsulated marigold extract, the ratio of oil to wall at 1:5 had the highest encapsulation efficiency and the highest lutein content. Extraction of lutein using coconut oil and the microwave method was the suitable method. The microencapsulated marigold extract can be applied for the development of functional ingredients.

Cognition is essential for daily activities and progressively deteriorates with age due to various factors leading to cognitive decline. This decline often begins with memory impairment and advances to broader cognitive dysfunctions. Resveratrol (RES), a natural phenolic compound found in red wine, has garnered significant attention for its potential to prevent cognitive decline. This review aims to synthesize the latest preclinical data on the cognitive restorative effects of RES. We highlight RES activities from cellular mechanisms to behavioral outcomes. Evidence from various cognitive impairment models demonstrates that RES exerts neuroprotective effects through multiple mechanisms, including anti-inflammatory, antioxidative, anti-apoptotic, and neurotrophic actions, all of which contribute to cognitive enhancement in behavioral studies. Despite the established role of RES in mitigating memory decline, our review identifies a critical gap in behavioral studies regarding cognitive flexibility. Further research in this domain is recommended. Additionally, species-specific pharmacokinetic differences may account for the inconsistencies between preclinical and clinical outcomes, particularly in rats and humans. We propose that formulations designed to delay gut metabolism through enterohepatic circulation could enhance the translational potential of RES. Furthermore, long-term studies are needed to determine the optimal dose capable of maximizing health benefits without raising toxicity during chronic use.

In this investigation, a number of phenoxyindole derivatives were designed, synthesized, and tested for their neuroprotective ability on SK-N-SH cells against Aβ₄₂-induced cell death and biologically specific activities involved in anti-Aβ aggregation, anti-AChE, and antioxidant effects. The proposed compounds, except compounds 9 and 10, could protect SK-N-SH cells at the IC₅₀ of anti-Aβ aggregation with cell viability values ranging from 63.05% ± 2.70% to 87.90% ± 3.26%. Compounds 3, 5, and 8 demonstrated striking relationships between the %viability of SK-N-SH cells and IC₅₀ values of anti-Aβ aggregation and antioxidants. No significant potency of all synthesized compounds against AChE was found. Among them, compound 5 showed the strongest anti-Aβ and antioxidant properties with IC₅₀ values of 3.18 ± 0.87 and 28.18 ± 1.40 μM, respectively. The docking data on the monomeric Aβ peptide of compound 5 demonstrated good binding at regions involved in the aggregation process, and the structural feature made it possible to be a superior radical scavenger. The most effective neuroprotectant belonged to compound 8, with a cell viability value of 87.90% ± 3.26%. Its unique mechanisms for enhancing the protective impact may serve additional purposes since it demonstrated mild biological-specific effects. In silico prediction of CNS penetration shows strong passive penetration ability across the blood–brain barrier from blood vessels to the CNS for compound 8. In light of our findings, compounds 5 and 8 appeared as potentially intriguing lead compounds for new therapeutic approaches to Alzheimer’s disease. More in vivo testing will be revealed in due course.

Mimosa pudica (M) and Abutilon indicum (A) are used as an antidiabetic mixture at a ratio of 1:1 (MA11)in traditional Thai medicine. However, the mechanisms by which these plants exhibit antidiabetic effects have not been clearly elucidated. In this study, RINm5F insulinoma cells were treated with 6 mM streptozotocin (STZ) for 1 h to induce cellular damage and generate an in vitro model of diabetes. Extracts from M and A and mixtures of M and A extracts contain several phytochemicals, including flavonoids, tannins and saponins. All the extract samples at a concentration of 1,000 µg/mL exhibited antioxidant activity without cytotoxicity to RINm5F and L6 myotube cells. Pretreatment with M or A or with a mixture of the two prevented STZ-induced RINm5F cell death in a concentration-dependent manner. The greatest recovery effect was found in MA12, followed by MA11 and MA21. In addition, the M and A extracts and the mixtures of M and A extracts (100,000 mg/mL) exhibited insulin secretory activity in RINm5F cells that was similar to that of glibenclamide. Furthermore, all the plant extracts induced glucose uptake in L6 myotube cells. The induction of glucose uptake by M, A, and mixtures of M and A was derived from the upregulation of GLUT1 and GLUT4 synthesis in L6 myotube cells. These results indicate that M. pudica and A. indicum are potential sources of antidiabetic agents. In conclusion, the antidiabetic formula of M and A at a ratio of 2:1 (MA21) has the greatest potential for therapeutic use as an antidiabetic herbal mixture.