Table 2.

Pharmacological effects of bile acid treatments on various ocular diseases.

Ocular Disease	Bile Acid /Agonist	Dose	Findings	References
Leber congenital amaurosis	TUDCA	Systemic injection; 500 mg/kg b.w./3 days	TUDCA is a potential agent in reducing ER stress, to prevent apoptosis, and preserve cones in the LCA model	[61]
Retinal detachment	TUDCA	Intraperitoneal injection; 500 mg/kg b.w.	TUDCA preserves photoreceptors after retinal detachment, inhibits caspase activity, and reduces ER and oxidative stress	[67]
Cataracts	TUDCA	Subcutaneous injection; 500 mg/kg body weight (b.w.)/day	TUDCA treatment alleviates cataract formation via the UPR-dependent pathway	[68]
Oxidative stress-induced retinal degeneration	TUDCA	Intraperitoneal injection; 500 mg/kg every 3 days	TUDCA produces modest preservation of outer nuclear layer thickness and rod function at P30. And significant preservation of cone cell number and cone function at P50	[74]
Retinal degeneration	TUDCA	Subcutaneous injection; 500 mg/kg b.w.	TUDCA greatly slowed retinal degeneration in LIRD, and rd10 mice protected photoreceptor and suppressed apoptosis	[75]
Rpgr-Associated Retinitis pigmentosa	TUDCA	Intraperitoneal injection; 500 mg/kg b.w.	TUDCA suppresses microglial activation, inhibits inflammation, and prevents photoreceptor degeneration	[79]
Retinal degeneration	TUDCA	Systemically injected; 500 mg/kg every 3 days from P6 to P30	TUDCA-treated rd10 retinas had fivefold more photoreceptors than vehicle-treated retinas. TUDCA treatments did not alter the retinal function or morphology of wild-type mice when administered to age-matched mice.	[80]
Retinal degeneration	TUDCA	Subcutaneous injection; 500 mg/kg b.w./ day	TUDCA treatment: reduces caspase 3 activation and apoptosis, slows the loss of photoreceptors and retinal function, and delays retinal damage	[83]
Retinal degeneration	TUDCA	Subcutaneous injection; 500 mg/kg b.w.	TUDCA inhibits photoreceptor degeneration and decreases visual impairments. TUDCA rectifies abnormalities in visual signal transmission	[84]
Diabetic Retinopathy	UDCA	Oral delivery, intragastric administration; 30 mg/kg b.w.	UDCA reverses the breakdown of the blood-retinal barrier and reduces retinal inflammation	[87]
Diabetic Retinopathy	UDCA	Intraperitoneal injection; 100 mg/kg/d b.w.	vascular integrity was improved and pericyte loss reduced in the retina of STZ-induced diabetic mice	[92]
Diabetic Retinopathy	UDCA	Subcutaneous injection / daily for P7-9 neonates; 100 mg/kg.	UDCA reduced the increased expression of angiogenic factors and inflammatory mediators (vascular endothelial growth factor, intercellular adhesion molecule-1, and monocyte chemotactic protein-1	[93]
Diabetic Retinopathy	INT-777 (semisynthetic bile acid) a TGR5 agonist	50 ng/μL, 5 μL was injected into the vitreous cavity	Upregulation or activation of TGR5 may inhibit RhoA/ROCK-dependent actin remodeling and represent an important therapeutic intervention for DR.	[96]
Choroidal neovascularization (CNV)	UDCA TUDCA	Intraperitoneal injection; UDCA 500 mg/kg, TUDCA 100 mg/kg,	The systemic administration of UDCA and TUDCA suppressed laser-induced CNV formation	[100]
Choroidal neovascularization (CNV)	UDCA	Oral delivery; 125 or 250 mg/kg b.w./day	UDCA inhibits CNV and promotes functional recovery in mice retinas	[101]
Retinopathy of prematurity	UDCA TUDCA GUDCA	Intraperitoneal injection; 50 mg/kg	UDCA decreased the extension of neovascular and avascular areas, whereas treatments with TUDCA and GUDCA showed no changes. UDCA also prevented reactive gliosis, preserved ganglion cell survival, and ameliorated OIR-induced blood-retinal barrier dysfunction.	[104]