Table 1.
In vivo biological and pharmacological activities of various pitaya extracts and pure compounds.
| Properties | Plant Part or Active Compounds | Species | Extraction | Experimental Model | Dose | Route of Administration | Methods of Analysis | Observations | References |
|---|---|---|---|---|---|---|---|---|---|
| Anxiolytic-like effects | Pulp and peel rich in maltotriose, quercetin-3-O-hexoside, and betalains bioactive compounds. | H. polyrhizus. | Ethanolic and aqueous extracts. | Zebrafish from both sexes. | 0.1 mg/mL or 0.5 mg/mL or 1.0 mg/mL, 20 μL. | Dissolved in the fish’s water. | Anxiolytic activities and toxicity assays. | The extracts showed no toxicity in the fish model and exerted significant anxiolytic effects as the fish reduced their permanence in the clear zone of the experimentation area compared to controls. | [21] |
| Metabolic effects | Betalain-rich pitaya pulp. | H. undatus. | Aqueous extract. | Streptozotocin-induced diabetes in male Sprague-Dawley rats. | 250 or 500 mg per kg body weight. | Intragastric gavage. | Pulse wave velocities, surgical procedures, and oxidative stress analyses. | The treated rats had reduced blood pressure, pulse wave velocities, and pulse pressures. | [22] |
| Betalain-rich pitaya juice. | H. polyrhizus. | Aqueous juice. | High-carbohydrate, high-fat diet-induced metabolic syndrome male Wistar rats. | 5% of red pitaya juice during the diet. | Oral by feeding. | Biochemical and physical tests, as well as histopathological assessments. | There was a significant reduction in the diastolic stiffness of the treated rats. Additionally, the treated rats presented reductions in the alkaline phosphatase and alanine transaminase serum concentrations. | [26] | |
| Pitaya’s juice. | H. polyrhizus. | Aqueous juice. | High-carbohydrate, high-fat diet-induced metabolic syndrome male Wistar rats. | 5% of red pitaya juice during the diet. | Oral by feeding. | Biochemical and physical tests, as well as genetic assessments. | During the treatment, the omental and epididymal fat of the rats increased. The pitaya treatment reversed the rats’ metabolic changes by up-regulating the obesity-related Pomc and Insr genes in the liver tissues. | [27] | |
| Pitaya’s peel purified betacyanins. | H. undatus. | Purified betacyanins. | High-fat diet-fed male C57BL/6J mice. | Different concentrations of different purified betacyanins. | Oral by feeding. | Biochemical and histopathological analyses. | The purified betacyanin ameliorated the AT’s hypertrophy, liver steatosis, body glucose intolerance, and the body’s IR. In the liver, the purified betacyanins also augmented the genetic expression of lipid metabolism genes, such as the Acox1, Cpt1b, Cpt1a, Insig1, PPARγ, AdipoR2, and Insig2 and of FGF-21 genes. The purified betacyanins alleviated the liver’s FGF21 resistance, decreased the liver’s fatty acid biosynthesis, and elevated the liver’s fatty acid oxidation. |
[28] | |
| Betacyanin-rich pitaya fruit. | H. polyrhizus. | Red pitaya’s fruit betacyanins. | Diet-induced obesity, liver steatosis, and insulin resistance C57BL/6J mice. |
200 mg/kg. | Intragastric gavage. | Biochemical, sequencing, and histological analyses. | The fruit protected the mice from obesity and its related metabolic disorders. There were improvements in the inflammatory statuses of the treated rats, as well as their gut microbiota (there was a decrease in the ratio of Firmicutes and Bacteroidetes and an increase in the relative amount of Akkermansia). | [31] | |
| Pitaya juice rich in polyphenols and flavonoids bioactive compounds. | H. undatus. | Aqueous juice. | Steatosis diet-induced obese C57BL/6J mice. | - | Oral by drinking. | Biochemical and histopathological assessments. | There were improvements in the FGF-21 resistance and lipid metabolisms of the treated rats. Additionally, the juice protected the rats against hepatic steatosis and IR. | [32] | |
| Concentrated Pitaya Pulp with seeds | H. polyrhizus. | Pulp with seed | Hyperlipidemic female C57BL/6 mice | 100, 200, and 400 mg/kg/day | Oral by feeding | Biochemical assessments. | There was an increase in the levels of HDL-c and a significant reduction in the levels of Total cholesterol, LDL, triglycerides, glycemia, AST, and ALT. | [23] | |
| Betacyanin-rich pitaya peel extract. | H. polyrhizus. | Methanolic extract. | Alcoholic-progressive liver disease ethanolic-diet C57BL/6 mice. | 500 and 1000 mg/kg of body weight. | Intragastric gavage. | Biochemical and histopathological assessments. | The treated group presented diminished liver injury and improved liver lipid metabolism via decreases in the SREBP-1 and increases in AMPK and PPAR-α protein expressions. The extract also inhibited the Nrf2 and CYP2E1 expression, reduced endotoxin levels, and decreased TLR4, MyD88, TNF-α, and IL-1β expression in the treated rats’ liver. | [25] | |
| Concentrated Pitaya Pulp with seeds | H. polyrhizus. | Pulp with seed | Hyperglycemic Zebrafish | 5–100% of pitaya pulp | Oral by feeding | Biochemical assessments. | There was a significant decrease in glycemia in all concentrations compared to placebo and with the use of metformin. | [24] | |
| Gastrointestinal | Pitaya’s fruit extract. | H. polyrhizus. | Ethanolic extract. | Balb/c mice induced colitis by trinitrobenzene sulphonic. | 1 g/kg. | Intraperitoneally. | Biochemical and histopathological analysis. | The extract exerted anti-inflammatory (decreases in the Ikb-a degradation and nuclear NF-kb protein levels) effects and prevented colitis development (reduced histological damage score) in the treated mice. | [29] |
| Wound-healing | Pitaya’s leaves, rind, fruit pulp, and flower extracts. | H. undatus. | Aqueous extract. | Streptozotocin diabetic Wistar rats | 200 µL/wound at concentrations of 0.05%, 0.1%, 0.2%, 0.4% and 0.5% twice daily. |
Topically. | Wound healing assays and DNA and protein estimation. | The use of the extract facilitated wound healing by enhancing tensile strength, hydroxyproline, DNA, total proteins, collagen content, and epithelization. | [30] |
ALT—Alanine transaminase; AMP—adenosine monophosphate; AMPK—AMP-activated protein kinase; AST—aspartate aminotransferase; AT—adipose tissue; CYP2E1—cytochrome P450 2E1; FGF-21—fibroblast growth factor 21; Ikb-a—Ikb kinase alpha; Insr—insulin receptor gene; IL-1β—interleukin 1 beta; IR—insulin resistance; MyD88—myeloid differentiation primary response gene 88; NF-kb—nuclear factor kappa b; Nrf2—nuclear factor erythroid 2-related factor 2; PPAR-α—peroxisome proliferator-activated receptor; Pomc—proopiomelanocortin gene; SREBP-1—hepatic sterol regulatory element-binding protein 1c; TLR4—toll-like receptor 4; TNF-α—tumor factor necrosis alfa.