Physiologically Active Molecules and Functional Properties of Soybeans in Human Health-A Current Perspective

Abstract

In addition to providing nutrients, food can help prevent and treat certain diseases. In particular, research on soy products has increased dramatically following their emergence as functional foods capable of improving blood circulation and intestinal regulation. In addition to their nutritional value, soybeans contain specific phytochemical substances that promote health and are a source of dietary fiber, phospholipids, isoflavones (e.g., genistein and daidzein), phenolic acids, saponins, and phytic acid, while serving as a trypsin inhibitor. These individual substances have demonstrated effectiveness in preventing chronic diseases, such as arteriosclerosis, cardiac diseases, diabetes, and senile dementia, as well as in treating cancer and suppressing osteoporosis. Furthermore, soybean can affect fibrinolytic activity, control blood pressure, and improve lipid metabolism, while eliciting antimutagenic, anticarcinogenic, and antibacterial effects. In this review, rather than to improve on the established studies on the reported nutritional qualities of soybeans, we intend to examine the physiological activities of soybeans that have recently been studied and confirm their potential as a high-functional, well-being food.

Keywords: active molecules; health benefit; soy functionality; soybean.

Figure 1

Nutritional value of carbohydrates, proteins, and fats (A), ratio of soluble and insoluble forms of carbohydrate (B), and composition of protein-derived amino acids (C) in soybeans [1].

Figure 2

Potential beneficial health effects of soybean molecules.

Figure 3

Chemical structure of the major classes of phenolic acids. Structures were drawn using Chem Spider tool.

Figure 4

Chemical structure of the major classes of isoflavones. Structures were drawn using Chem Spider tool.

Figure 5

Schematic of multiple signaling pathways involved in isoflavone-induced cancer cell death [30]. Wnt-3α, a protein of the Wnt family, plays critical roles in regulating pleiotropic cellular functions [30]. AR, androgen receptor; Akt, a serine/threonine-specific protein kinase known as a protein kinase B; BAD, Bcl2-associated agonist of cell death; GSK-3β, glycogen synthase kinase 3 beta; EGF, epidermal growth factor; EGFR, epidermal growth factor receptor; TCF, T-cell specific transcription factor; IKK, IκB kinase; p53, tumor protein-53; β-catenin, a core component of the cadherin protein complex; PI3K, phosphatidylinositol-3-kinase; NF-κB, nuclear factor kappa light-chain-enhancer of activated B cells; Notch, a family of type-1 transmembrane proteins; →, activation; ⊥, inactivation. Figure adapted from Li, Y. et al. [30].

Figure 6

Mechanism of action of soybean isoflavones [12,30]. ER, endoplasmic reticulum; VEGF, vascular endothelial growth factor.

Figure 7

Structure and schematic representation of clinical properties of phytic acid [68,71].

Figure 8

Biological activities of protease inhibitors (left panel) and schematic representing major pharmacological activities of soybean (right panel). Figure adapted from Srikanth, S. et al. [74].

Figure 9

The cellular and molecular targets for anticancer (left panel) and protective health benefits of lignan (right panel). Cancer metastatic potentials are downregulated by blocking the cytoskeleton-driven cell mobility precursors. Regulation of cell differentiation and proliferation and cell cycle arrest can also interfere with survival and growth of cancer cells. Antiangiogenic starvation of tumor cells and apoptotic induction contribute to tumor progression, survival, and invasion potentials. Inhibiting various cellular signaling pathways associated with downstream intracellular kinases, including AKT, ERK, and mitogen kinases, regulates cellular metabolic pathways, triggering the suppressed tumor growth and progression [91]. In addition, lignan-containing diets or supplements can enhance general health and prevent various diseases. Cdc42, cell division control protein 42 homolog; AKT1, RAC-alpha serine/threonine-protein kinase; p-FAK, phosphorylated focal adhesion kinase; GADD45A, growth arrest and DNA damage inducible alpha; IGFR, insulin-like growth factor 1 receptor; p-ERK, phosphorylated extracellular-signal-regulated kinase; p-paxillin, phosphorylated focal adhesion-associated adaptor protein; RhoA, Ras homolog family member A; Rac1, Ras-related C3 botulinum toxin substrate 1; MMP2/9/14, matrix metalloproteinase-2, -9, and -14; FoxM1, forkhead box protein M1; PCNA, proliferating cell nuclear antigen; Cyclin, a protein family that controls the progression of a cell through the cell cycle; MKI67, marker of proliferation Ki-67; CDK2, cyclin-dependent kinase-2; CDKN3, cyclin-dependent kinase inhibitor 3; p-Src, phosphorylated proto-oncogene tyrosine-protein kinase; PDGF, platelet-derived growth factor; p-AKT, phosphorylated protein kinase B; p-GSK3β, phosphorylated glycogen synthase kinase 3 beta; p-MDM2, phosphorylated E3 ubiquitin-protein ligase; EGFR, epidermal growth factor receptor; ERα/β, estrogen receptor alpha/beta; FASN, fatty acid synthase; CYP3A4, cytochrome P450 3A4; COX-1/2, cyclooxygenase-1/2; E2F, E2 factor; E2F1, E2F transcription factor 1; KLK3/4, prostate-specific antigen 3/4; Survivin (BIRC5), an inhibitor of apoptosis protein; RBL1, retinoblastoma-like protein 1; VEGF, vascular endothelial growth factor; VEGFR2, vascular endothelial growth factor receptor-2; Cytochrome C, a heme protein localized in the compartment between the inner and outer mitochondrial membranes; PARP, poly (ADP-ribose) polymerase; Caspase-3, an endo-protease which regulates inflammatory and apoptotic signaling networks; p-p53, phosphorylated tumor suppressor p53; Bcl-2, B-cell lymphoma-2 as an apoptotic regulator. Figure adapted from De Silva, S.F. et al. [91].

Figure 10

Chemical structure and in vitro cholesterol-lowering mechanism of saponin (A), and schematic representation of plausible anticancer mechanism of saponin derivatives at the cellular level (B) [95]. p21, a potent cyclin-dependent kinase inhibitor; β-catenin, a core component of the cadherin protein complex; COX, cyclooxygenase; PARP, poly (ADP-ribose) polymerase. →, activation; ⊥, inactivation; ---, indirect activation. Figure adapted from Podolak, I. et al. [95].

Figure 11

Chemical structures of soybean oligosaccharides comprising stachyose and raffinose (A) and effect of functional oligosaccharides on high blood pressure (B). Figure adapted from Zhu, D. et al. [132].

Figure 12

Mechanism of cholesterol degradation through lactostatin (IIAEK)-driven CYP7A1 expression in hepatic carcinoma HepG2 cell line. CYP7A1, cytochrome P450 monooxygenase; CAMK, calmodulin kinase; ERK, extracellular-signal-regulated kinase; MEK, mitogen-activated protein kinase kinase; Ras, a small GTPase protein; Raf-1, proto-oncogene serine/threonine-protein kinase; TF, transcription factor. Figure adapted from Nagaoka, S. [150].

Figure 13

Regulation of angiotensin-converting enzyme (ACE) in blood pressure by soybean protein. ACE catalyzes the degradation of bradykinin, a blood lowering-protein/peptide in the kallikrein–kinin system. Inhibition of ACE is postulated to be an effective medical target in the treatment of hypertension. Hypertension is a key factor associated with several diseases, such as cardiovascular disease and stroke [5]. Figure adapted from Chatterjee, C. et al. [5].

Figure 14

Structure of the major phospholipids (PLs) found in soybean lecithin (left panel) and action mode of PLs in liver diseases (right panel) [154].

Figure 15

Schematic illustration of the CLA-regulated biological pathway during carcinogenic, adipose, diabetic, and cardiovascular diseases. CLA conjugated to nuclear receptors such as PPARs combines with a counterpart nuclear receptor named RXR to transcriptionally downregulate the target genes related to lipid metabolism including cellular differentiation of adipocytes, cancer cells, inflammatory cells, and pancreatic cells [184]. CLA, conjugated linoleic acid; PPAR, peroxisome proliferator-activated receptor; PPRE, peroxisome proliferator responsive element; RXR, retinoid X receptor. Figure adapted from Yang, B. et al. [184].

Figure 16

Insulin-resistant effects of pinitol. IRS, insulin receptor substrate; p85/p110, phosphoinositide-3-kinase-alpha subunits; PI3K, phosphoinositide-3-kinase; PIP2/3, probable plasma membrane intrinsic aquaporin protein; PDK, phosphoinositide-dependent protein kinase; AKT, protein kinase B; SREBP1c, sterol regulatory element-binding protein 1; GSK3, glycogen synthase kinase 3; PDE3B, cyclic nucleotide phosphodiesterase 3B; mTORC1, mechanistic target of rapamycin (mTOR) complex 1; FOXO, the O class of the forkhead box class transcription factors. Figure adapted from Antonowski, T. et al. [196].