Table 3.

Biological activity of purslane polysaccharides and their underlying mechanisms of actions.

Biological Activity	Polysaccharide Name	In Vitro or In Vivo	Indicated Concentration	Models/Test System	Action or Mechanism	Ref.
Antifatigue effects	POP-X	In vivo	75, 150 and 300 mg/kg	Male KM mice	POP prolongs riding time and extreme swimming time in mice, reduces blood lactate and serum urea nitrogen levels and increases liver and muscle glycogen content.	[17]
Antidiabetic effects	POP-L	In vitro	0.5 mg/mL	INS-1 cells	POP increases mitochondrial membrane potential and ATP production; depolarises cell membrane potential (MP), intracellular Ca2+ levels ([Ca2+]) and Nav1.3 expression levels; and decreases Nav1.7 expression levels.	[26]
	CPOP	In vivo	100, 200 and 400 mg/kg	SD rats	CPOP appears to significantly reduce FBG, TNF-6, IL-6 and MDA levels and increase FINS, ISI and ROS levels in diabetic rats.	[24]
Antiviral effects	RP	In vitro	234 mg	Cells and Viruses V ero and Madin–Darby canine kidney (MDCK) cells were grown in minimal essential medium (MEM) containing 5% fetal bovine serum (FBS)	RP has been shown to exert potential anti-HSV-2 activity by inhibiting viral penetration without inhibiting viral adsorption.	[19]
Antitumor effects	POP1(POP1-s1, POP1-s2, POP1-s3 and POP1-s4)	In vitro	100–2000 μg/mL	HepG2 and Hela cells	Inhibits the growth of Hela cells in S-phase and induces apoptosis through cell cycle arrest.	[29]
	POL-P3b	In vitro	100 or 200 mg/mL	HeLa cells	POL-P3b induces apoptosis in HeLa cells by upregulating Bax levels and downregulating Bcl-2 protein levels, while inducing apoptosis in part by regulating the Bcl-2 family. The target of POL-P3b is probably TLR4 on HeLa cells, and POL-P3b induces apoptosis through activation of the TLR4/NF-kB pathway.	[36]
	POP-S	In vivo	25, 50, and 100 mg/kg	ICR mice	POP significantly inhibits the growth of transplantable sarcoma 180, increases the number of white blood cells (WBC) and CD4+ T lymphocytes and increases the CD4+/CD8+ ratio. In addition, oral administration of POP significantly increases the number of peripheral blood leukocytes and reduces serum AST, ALT, BUN and creatinine levels in tumor-bearing mice.	[22]
	POL-P3b	In vivo	50, 100 and 200 mg/kg	Female KM mice	Pol-p3b induces tumor-induced apoptosis in DC cells by stimulating the TLR4-PI3K/AKT-NF-κB signaling pathway.	[37]
	POL-P3b	In vivo	50 µg/mL and 100 mg/mL	BALB/c female mice	The mechanism of action may be related to the enhancement of specific antitumor immune responses involving the TLR4/MyD88/NF-κB signaling pathway.	[38]
	POL-P3b	In vitro and in vivo	250, 500 and 1000 μg/mL 50, 100 and 200 mg/kg	HeLa and U14 cells, Female KM mice	POL-P3b inhibits the growth of cervical cancer cells in vitro and in vivo, and also significantly inhibits tumor growth in U14 mice.	[18]
Anticolitis effects	POLP	In vivo	0.75, 0.5 and 0.25 g/mL	KM mice	POLP exerts its protective effect through regulation of the IL-6/STAT3/COX-2 pathway.	[23]
Immunomodulatory effects	PSPO (SePSPO-1, SePSPO-2)	In vitro	753.8 and 1325.1 mg/kg	Female BALB/c	The higher the degree of selenylation of PSPO, the stronger the immunomodulatory effect on model cells, the increased phagocytosis of macrophages and the increased secretion of cytokines related to immunity.	[20]
	POL-P3b	In vivo	250, 500 and 1000 μg/mL	Recombinant mouse GM-CSF, mouse CD11c, FITC antimouse CD80, FITC antimouse CD83, PE antimouse CD86 and PE antimouse MHC-II	The expression of TLR-4 is significantly increased in POL-P3b-treated dc, which may induce dc maturation through TLR-4, and this has important implications for the molecular mechanism of POL-P3b immune enhancement.	[39]
	Purslane polysaccharide	In vitro and in vivo	1, 5, 10, 20 and 40 μg/mL	Wistar rats; thymocytes	Purslane polysaccharides scavenge excess free radicals and boost the immune system.	[16]
Anti-lead poisoning effects	POP-T	In vitro and in vivo	600 mg/kg/day	PC12 cells and rats	POP is protective against pb-induced oxidative toxicity in PC12 cells by reducing ROS production and increasing cell viability and also attenuates cognitive deficits in brain CA1 and DG regions and significantly reverses pb-induced spinal deficits in brain CA1 and DG regions.	[15]