Anti-Inflammatory Activity of Pequi Oil (Caryocar brasiliense): A Systematic Review.

Disorders in the inflammatory process underlie the pathogenesis of numerous diseases. The utilization of natural products as anti-inflammatory agents is a well-established approach in both traditional medicine and scientific research, with studies consistently demonstrating their efficacy in managing inflammatory conditions. Pequi oil, derived from Caryocar brasiliense, is a rich source of bioactive compounds including fatty acids and carotenoids, which exhibit immunomodulatory potential. This systematic review aims to comprehensively summarize the scientific evidence regarding the anti-inflammatory activity of pequi oil. Extensive literature searches were conducted across prominent databases (Scopus, BVS, CINAHL, Cochrane, LILACS, Embase, MEDLINE, ProQuest, PubMed, FSTA, ScienceDirect, and Web of Science). Studies evaluating the immunomodulatory activity of crude pequi oil using in vitro, in vivo models, or clinical trials were included. Out of the 438 articles identified, 10 met the stringent inclusion criteria. These studies collectively elucidate the potential of pequi oil to modulate gene expression, regulate circulating levels of pro- and anti-inflammatory mediators, and mitigate oxidative stress, immune cell migration, and cardinal signs of inflammation. Moreover, negligible to no toxicity of pequi oil was observed across the diverse evaluated models. Notably, variations in the chemical profile of the oil were noted, depending on the extraction methodology and geographical origin. This systematic review strongly supports the utility of pequi oil in controlling the inflammatory process. However, further comparative studies involving oils obtained via different methods and sourced from various regions are warranted to reinforce our understanding of its effectiveness and safety.

Pequi oil (Caryocar brasilense Cambess.) nanoemulsion alters cell proliferation and damages key organelles in triple-negative breast cancer cells in vitro.

Pequi oil is extracted from the fruit of a Brazilian native plant (Caryocar brasiliense Camb) that contains some molecules with anticancer potential. Due to its hydrophobic property, the administration of pequi oil associated with nanoemulsion systems represents a successful strategy to improve oil bioavailability. Breast cancer is the most frequent type of cancer among women and conventional therapies used are frequently associated with several side effects. Thus, the aim of this study was to investigate the effects of pequi oil-based nanoemulsion (PeNE) on triple-negative breast cancer cells (4T1), in vitro. PeNE presented a dose- and time-dependent cytotoxic effect with lower IC50 than free pequi oil after 48 h of exposure (p < 0.001). At 180 µg/mL, PeNE demonstrated numerous cell alterations, when compared to free pequi oil, such as morphological alterations, reduction in cell proliferation and total cell number, damage to plasmatic membrane, induction of lysosomal membrane permeability and depolarization of mitochondrial membrane, alteration of intracellular ROS production and calcium level, and increase in phosphatidylserine exposure. Taken together, the results suggest an interesting induction of cell death mechanisms involving a combined action of factors that impair nucleus, mitochondria, lysosome, and ER function. In addition, more pronounced effects were observed in cells treated by PeNE at 180 µg/mL when compared to free pequi oil, thereby reinforcing the advantages of using nanometric platforms. These promising results highlight the use of PeNE as a potential complementary therapeutic approach to be employed along with conventional treatments against breast cancer in the future.

In Vivo Efficacy and Toxicity of Curcumin Nanoparticles in Breast Cancer Treatment: A Systematic Review.

Breast cancer is one of the most prevalent types of malignant tumors in the world, resulting in a high incidence of death. The development of new molecules and technologies aiming to apply more effective and safer therapy strategies has been intensively explored to overcome this situation. The association of nanoparticles with known antitumor compounds (including plant-derived molecules such as curcumin) has been considered an effective approach to enhance tumor growth suppression and reduce adverse effects. Therefore, the objective of this systematic review was to summarize published data regarding evaluations about efficacy and toxicity of curcumin nanoparticles (Cur-NPs) in in vivo models of breast cancer. The search was carried out in the databases: CINAHL, Cochrane, LILACS, Embase, FSTA, MEDLINE, ProQuest, BSV regional portal, PubMed, ScienceDirect, Scopus, and Web of Science. Studies that evaluated tumor growth in in vivo models of breast cancer and showed outcomes related to Cur-NP treatment (without association with other antitumor molecules) were included. Of the 528 initially gathered studies, 26 met the inclusion criteria. These studies showed that a wide variety of NP platforms have been used to deliver curcumin (e.g., micelles, polymeric, lipid-based, metallic). Attachment of poly(ethylene glycol) chains (PEG) and active targeting moieties were also evaluated. Cur-NPs significantly reduced tumor volume/weight, inhibited cancer cell proliferation, and increased tumor apoptosis and necrosis. Decreases in cancer stem cell population and angiogenesis were also reported. All the studies that evaluated toxicity considered Cur-NP treatment to be safe regarding hematological/biochemical markers, damage to major organs, and/or weight loss. These effects were observed in different in vivo models of breast cancer (e.g., estrogen receptor-positive, triple-negative, chemically induced) showing better outcomes when compared to treatments with free curcumin or negative controls. This systematic review supports the proposal that Cur-NP is an effective and safe therapeutic approach in in vivo models of breast cancer, reinforcing the currently available evidence that it should be further analyzed in clinical trials for breast cancer treatments.

Lycopene-rich extract from red guava (Psidium guajava L.) displays cytotoxic effect against human breast adenocarcinoma cell line MCF-7 via an apoptotic-like pathway.

This study investigated a lycopene-rich extract from red guava (LEG) for its chemical composition using spectrophotometry, mass spectrometry, attenuated total reflectance-fourier transform infrared spectroscopy (ATR-FTIR), and computational studies. The cytotoxic activity of LEG and the underlying mechanism was studied in human breast adenocarcinoma cells (MCF-7), murine fibroblast cells (NIH-3T3), BALB/c murine peritoneal macrophages, and sheep blood erythrocytes by evaluating the cell viability with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) method and flow cytometry. Spectrophotometry analysis showed that LEG contained 20% of lycopene per extract dry weight. Experimental and theoretical ATR-FTIR suggests the presence of lycopene, whereas MS/MS spectra obtained after fragmentation of the molecular ion [M]+• of 536.4364 show fragment ions at m/z 269.2259, 375.3034, 444.3788, and 467.3658, corroborating the presence of lycopene mostly related to all-trans configuration. Treatment with LEG (1600 to 6.25µg/mL) for 24 and 72h significantly affected the viability of MCF-7 cells (mean half maximal inhibitory concentration [IC50]=29.85 and 5.964µg/mL, respectively) but not NIH-3T3 cells (IC50=1579 and 911.5µg/mL, respectively). Furthermore LEG at concentrations from 800 to 6.25µg/mL presented low cytotoxicity against BALB/c peritoneal macrophages (IC50≥800µg/mL) and no hemolytic activity. LEG (400 and 800µg/mL) caused reduction in the cell proliferation and induced cell cycle arrest, DNA fragmentation, modifications in the mitochondrial membrane potential, and morphologic changes related to granularity and size in MCF-7 cells; however, it failed to cause any significant damage to the cell membrane or display necrosis or traditional apoptosis. In conclusion, LEG was able to induce cytostatic and cytotoxic effects on breast cancer cells probably via induction of an apoptotic-like pathway.