Nanotechnology has revolutionized drug delivery, particularly through nanoformulations of phytoconstituents, enhancing their therapeutic potential. Despite their broad bioactivities, plant-based compounds often suffer from poor bioavailability and stability. Nanoformulations address these limitations by improving solubility, targeted delivery, and controlled release. This approach opens new possibilities for treating chronic diseases like cancer, diabetes, and neurodegenerative disorders. This review aims to examine recent advancements in nanotechnology-based formulation strategies designed to enhance the delivery, stability, and therapeutic efficacy of phytochemicals and also discusses regulatory issues, safety concerns, scalability, and cost-effectiveness. Emphasis was placed on nanoformulation techniques employed for key phytoconstituents such as curcumin, resveratrol, epigallocatechin gallate, and quercetin. The most commonly employed nanocarriers included polymeric nanoparticles, solid lipid nanoparticles, and liposomes. These formulations significantly improved the solubility, stability, and controlled release profiles of phytochemicals. In vitro and in vivo studies demonstrated enhanced anti-inflammatory, anticancer, and antioxidant activities. Moreover, surface-modified and targeted nanoparticles showed promise in increasing site-specific targeting and enhancing bioavailability of the encapsulated compounds. Nanoformulations present a promising strategy for overcoming the pharmacokinetic limitations of phytochemicals. Despite encouraging preclinical results, further studies are needed to address issues related to long-term safety, clinical efficacy, and regulatory approval for successful clinical translation.

Objective: To investigate effect of oleanolic acid (OA) on atherosclerosis and its related mechanisms.

Methods: Human umbilical vein endothelial cells (HUVECs) were injured by oxidized low-density lipoprotein for 24 h and treated with OA, and the levels of cell proliferation, migration, adhesion, and apoptosis were evaluated by BrdU staining, scratch healing assay, monocyte-endothelial cell adhesion assay and flow cytometry. The mice were fed with a high-fat diet to induce an atherosclerosis model, and treated with OA by gastric gavage. The mice were divided into the control group, the model group, and the OA administration group. The blood lipid and plaque formation in mice were detected. In addition, oxidative stress and mitochondrial structure and function changes in cells and mice were evaluated by transmission electron microscopy, JC-1 fluorescent probe, and Western blotting assays. The expression levels of proteins in the AMPK/Drp1 pathway were examined through Western blot.

Results: OA markedly increased cell viability and migration rate of HUVECs, and decreased the adhesion rate of THP-1 cells and the apoptosis rate. OA significantly reduced serum lipid levels, such as total cholesterol and triglyceride, in mice and inhibited plaque formation in the aorta. OA also significantly increased the content of superoxide dismutase and catalase, alleviated mitochondrial damage, such as mitochondrial swelling and mitochondrial cristae reduction, reduced the number of mitochondria, increased adenosine triphosphate content, and significantly reduced p-Drp1 (Ser616)/Drp1, MFF and FIS1 levels, increased p-AMPK/AMPK levels, activated AMPK, and then regulated DRP1 activity.

Conclusions: OA activates AMPK, which in turn regulates the activity of DRP1 to restore normal mitochondrial dynamics and reduce atherosclerosis.

Objective: To study the potential of Pituranthos chloranthus essential oil (PC) as a chemoprotective agent.

Methods: In the in vitro study, cell proliferation were determined in CT26, SW620, and SW480 cells. Cells were exposed to in-creasing concentrations of PC (0, 6.25, 12.5, 25, 50, 100, and 200 μg/mL). Combination index was calculated by applying the Chou-Talalay method, apoptopsis was analyzed by annexin V/propidium iodide staining, reactive oxygen species accumulation, and the Δψm drop were also assessed. In the in vivo study, mice were divided into 5 groups: the normal control group, the CT26 tumor-bearing group, the CT26 tumor-bearing mice+PC group, the CT26 tumor-bearing mice+cisplatin group, and the CT26 tumor-bearing mice+cisplatin+PC group. Organ coefficients and tumor volume were calculated. Alanine aminotransferase, aspartate aminotransferase, creatinine, and tumor necrosis factor-a levels were assessed.

Results: Cisplatin with PC induced a synergistic effect, allowing for reduced cisplatin dose while maintaining the same therapeutic efficacy. PC-cisplatin combinations inhibited cell viability by significantly inducing apoptosis, increasing reactive oxygen species accumulation and reducing mitochondrial membrane potential. Co-treatment with cisplatin and PC restored organ coefficients, reduced tumor volume, and alleviated nephrotoxicity in CT26 tumor-bearing mice by restoring kidney function markers and ameliorating kidney inflammation status.

Conclusions: PC shows a chemoprotective potential by enhancing the antitumor effect of cisplatin while alleviating its side effects.