Table 3.
Multifunctional platforms loaded with chemical drugs.
| Loaded drug | Mechanism | Diseases and Curative Effects | References |
|---|---|---|---|
| 17β-estradiol | Estrogen. Significantly inhibits IUA-increased TGF-β1, epidermal growth factor and PDGF-BB levels; promotes ESR1 levels; promotes PI3K/Akt and ERK1/2 signaling activation, and inhibits endoplasmic reticulum stress. | Postoperative estrogen therapy can be used to prevent recurrent adhesions; estrogen can increase the number of cells in endometrial damage and promote endometrial regeneration; inhibit endoplasmic reticulum stress-related apoptosis | [145] |
| Sitagliptin | Dipeptidyl peptidase IV (DPP4) inhibitor. Promotes stem cell homing and enrichment to the site of tissue damage | Inhibits the expression of DIO2, a marker gene of senescent decidual cells, increases endometrial-media embryonic stem cells, and reduces decidual senescence | [166] |
| Pentoxyphene | Medications that increase endometrial blood flow | Treats endometrial damage | [167] |
| Tocopherol | |||
| Sildenafil | |||
| Vc | Regulatory factor. Promotes stem cell survival, promotes endometrial recovery, promotes keratin, vWF expression recovery, reduces IL-1β | Attenuates the cytotoxic effect of PF-127, promotes cell survival and growth during encapsulation of rat bone marrow mesenchymal stem cells, and promotes intimal regeneration. | [114] |
| Mitomycin C | Antibiotics. | Inhibits the cell viability of endometrial stromal cells, promotes G1 cell cycle arrest and apoptosis, and inhibits the synthesis and secretion of type I collagen. | [168] |
| Metformin | Anti-diabetic drugs. | Inhibits ER stress-induced apoptosis through PI3K/Akt and ERK1/2 pathways. | [169] |
| Silver ions | Fungicide. Exhibits anti-infective effect. | Works synergistically with other ingredients facilitating endometrial regeneration, fertility restoration, and live birth of offspring | [170] |