Therapeutic Potential of Medicinal Plants and Their Phytoconstituents in Diabetes, Cancer, Infections, Cardiovascular Diseases, Inflammation and Gastrointestinal Disorders

Abstract

Conditions like diabetes mellitus (DM), cancer, infections, inflammation, cardiovascular diseases (CVDs), and gastrointestinal (GI) disorders continue to have a major global impact on mortality and morbidity. Medicinal plants have been used since ancient times in ethnomedicine (e.g., Ayurveda, Unani, Traditional Chinese Medicine, and European Traditional Medicine) for the treatment of a wide range of disorders. Plants are a rich source of diverse phytoconstituents with antidiabetic, anticancer, antimicrobial, antihypertensive, antioxidant, antihyperlipidemic, cardioprotective, immunomodulatory, and/or anti-inflammatory activities. This review focuses on the 35 plants most commonly reported for the treatment of these major disorders, with a particular emphasis on their traditional uses, phytoconstituent contents, pharmacological properties, and modes of action. Active phytomolecules with therapeutic potential include cucurbitane triterpenoids, diosgenin, and limonoids (azadiradione and gedunin), which exhibit antidiabetic properties, with cucurbitane triterpenoids specifically activating Glucose Transporter Type 4 (GLUT4) translocation. Capsaicin and curcumin demonstrate anticancer activity by deactivating NF-κB and arresting the cell cycle in the G2 phase. Antimicrobial activities have been observed for piperine, reserpine, berberine, dictamnine, chelerythrine, and allitridin, with the latter two triggering bacterial cell lysis. Quercetin, catechin, and genistein exhibit anti-inflammatory properties, with genistein specifically suppressing CD8+ cytotoxic T cell function. Ginsenoside Rg1 and ginsenoside Rg3 demonstrate potential for treating cardiovascular diseases, with ginsenoside Rg1 activating PPARα promoter, and the PI3K/Akt pathway. In contrast, ternatin, tannins, and quercitrin exhibit potential in gastrointestinal disorders, with quercitrin regulating arachidonic acid metabolism by suppressing cyclooxygenase (COX) and lipoxygenase activity. Further studies are warranted to fully investigate the clinical therapeutic benefits of these plants and their phytoconstituents, as well as to elucidate their underlying molecular mechanisms of action.

Keywords: cancer; cardiovascular diseases; diabetes; ethnomedicine; gastrointestinal disorders; infection; inflammation; medicinal plants; phytoconstituents.

Figure 1

Flowchart illustrating the literature search and screening process for this review.

Figure 2

Schematic diagram illustrating the various pharmacological actions of medicinal plants: Medicinal plants exhibit their antidiabetic effects via improvement of β-cell function and insulin secretion; anticancer properties by inhibiting viral gene expression and cell wall proliferation; antimicrobial effects by inhibiting bacterial cell wall and protein synthesis; anti-inflammatory effects by inhibiting the COX enzyme in blood vessels and ROS formation, inducing free radical scavenging activity in inflamed cells via suppression of TNF-α, IL-1β, and other inflammatory cytokines in adipose tissue; anti-ulcer properties by inhibiting H⁺/K⁺-ATPase, increasing CCK, GLP-1, and gastric motility, and regulating mucus production.

Figure 3

Schematic diagram illustrating the organ/tissue targeted by antidiabetic medicinal plants. Antidiabetic medicinal plants reduce glucose absorption in the small intestine and glucose production in the liver, increase insulin secretion from pancreatic β-cells, and promote glucose uptake in the skeletal muscle and adipose tissue.

Figure 4

Schematic diagram illustrating the organ/tissue targeted by anticancer medicinal plants: Anticancer medicinal plants suppress the uncontrolled proliferation of cells during division, the synthesis of proteins in ribosomes, DNA protein binding of cancer cells, and arrest of the cancer cell cycle by inhibiting cell division.

Figure 5

Schematic diagram illustrating the organ/tissue targeted by antimicrobial medicinal plants: Antimicrobial medicinal plants inhibit cell wall synthesis, depolarize bacterial cell membranes, inhibit protein synthesis in bacterial ribosomes, and suppress nucleic acid synthesis in the bacterial cell.

Figure 6

Schematic diagram illustrating the organ/tissue targeted by anti-inflammatory medicinal plants: Anti-inflammatory medicinal plants inhibit the COX enzyme in blood vessels, attenuate ROS formation in mitochondria, possess free radical scavenging activity in inflamed cells, and inhibit TNF-α, IL-1β, and other inflammatory cytokines in adipose tissue.

Figure 7

Schematic diagram illustrating the mechanisms of action of cardioprotective medicinal plants: Cardioprotective medicinal plants enhance NO and cGMP levels, promote vasodilation, and improve endothelial function. They regulate cellular survival and vascular smooth muscle cell proliferation via the PI3K/Akt pathway. Additionally, they upregulate key antioxidant enzymes, including HO-1, SOD, CAT, and GSH-Px, thereby enhancing cellular antioxidant capacity. These plants also activate Ca²⁺-gated potassium channels and inhibit the Na⁺/Ca²⁺ exchanger to protect against myocardial ischemia.

Figure 8

Schematic diagram illustrating the organ/tissue targeted by anti-ulcer medicinal plants: Anti-ulcer medicinal plants inhibit H⁺/K⁺-ATPase in the parietal cells of the stomach, regulate mucus formation of the stomach lining, stimulate gastric motility in the small intestine, and increase the release of CCK and GLP-1 by intestinal cells.

Figure 9

Phytoconstituents with antidiabetic, anticancer, antimicrobial, anti-inflammatory, cardioprotective and gastroprotective activities and their mechanisms of action: Phytoconstituents exhibit antidiabetic effects by increasing GLUT-4 translocation through AMPK activation, inhibiting DPP-IV, α-amylase, and α-glucosidase activity; anticancer effects by inhibiting the PI3K/AKT/mTOR, PI3K/AKT/FOXO pathways, STAT3 mediated HIF-1α/VEGF/Rho-GTPases and inactivating IGF-1R/p-Akt signaling transduction; antibacterial effects by inhibiting DNA gyrase, RNA polymerase, topoisomerase I, II, IV, and IA, cell division, and protein synthesis; anti-inflammatory effects by increasing the action of SOD, catalase (CAT), GPx, GR, GST and γ-GCS, suppressing COX and lipoxygenase and inhibiting IL-1β, IL-6, TNF-α, PGE2, and NF-κB activity; cardioprotective effects through activation of PI3K/Akt and cholinergic pathway, PPARα promoter, Ca²⁺-gated potassium channels and increasing the phosphorylation of Nrf2; gastroprotective effects by altering Na+K+ATPase activity, stimulating PPARγ pathway and inhibiting 5-HT3 and 5-HT4 receptors.