Treatment of experimental autoimmune uveoretinitis with different natural compounds

Abstract

Uveitis is an important eye disease that potentially causes loss of sight. Although extensive studies have been conducted on uveitis, the exact pathogenesis remains to be determined. The effects of treatment with natural compounds on an experimental autoimmune uveoretinitis (EAU) rat model were examined in the present study. A total of 25 rats were divided into 5 groups: Alkaloids (n=5), saponins (n=5), flavonoids (n=5), phenols (n=5), and the normal saline group (n=5). The rats in each group were treated with an intraperitoneal injection of proper alkaloids (berberine hydrochloride), saponins (steroidal saponins), flavonoids (baicalein), or phenols (chlorogenic acid) or physiological saline, respectively. The rats' aqueous humour and crystalline lens was then observed under the slit lamp periodically, looking for signs of inflammation. After 2 weeks, the rats were sacrificed and the degree of pathological changes on their eyeballs under different treatment methods were determined using an optical microscope. The expression of the interleukin (IL)-17 gene in the ocular tissues of the rats was assessed via RT-PCR and western blot analysis. Apoptosis on the rats' retinal tissues was detected using flow cytometry. The results showed that rats injected with phenols (chlorogenic acid) had serious ocular vascular dilatation, iris hemorrhage and purulent exudation; those injected with alkaloids (berberine hydrochloride) and flavonoids (baicalein) had a more mild form of inflammation; and those administered saponins (steroidal saponins) had only mild inflammation signs. Following detection of IL-17 mRNA and protein expression levels in the ocular tissues of rats of the five groups, it was found that their expression was lowest in the saponin-treated group and the other differences in expression were all statistically significant (P<0.05). A comparison with other groups revealed that cell apoptosis in the eyes of rats in the saponin group was the most prominent, reflecting a beneficial decrease in the amount of inflammatory cells on the lesion. Based on these findings, natural compounds such as saponins (steroidal saponins), alkaloids (berberine hydrochloride), and flavonoids (baicalein), but not phenols (chlorogenic acid), can inhibit the clinical symptoms of EAU in rats to a certain extent and reduce cell apoptosis. The most promising results in the present study were obtained using steroidal saponins.

Anti‐inflammatory and immune‐modulatory impacts of berberine on activation of autoreactive T cells in autoimmune inflammation

“…151,152 Of note, berberine has been found to ameliorate ocular manifestations of EAU in the experimental model. 76,153 Berberine-treated cussed with detail in the previous section). 76 Similar results were also reported by another study on berberine-treated EAU rats.…”

Potential Molecular Mechanisms of Plantain in the Treatment of Gout and Hyperuricemia Based on Network Pharmacology

“…Plantain can reduce serum uric acid level of hyperuricemia mice by inhibiting XOD activity and can improve swelling and activity of gouty arthritis [ 39 – 41 ]. Studies have shown that the compounds baicalein [ 42 ], baicalin [ 35 ], sitosterol [ 43 ], stigmasterol [ 44 ], and luteolin [ 45 ] can inhibit the level of IL-17. In conclusion, plantain has a good therapeutic effect on gouty arthritis and hyperuricemia; however, the mechanism of plantain in the treatment of gouty arthritis and hyperuricemia disease through IL-17 signaling pathway needs to be further explored.…”

“…Baicalein can also prevent retinal ischemia by reducing the levels of HIF-1 α , VEGF, and MMP-9 [ 53 ]. It can also reduce the expression of IL-17 protein to treat autoimmune uveoretinitis [ 42 ]. Baicalein can inhibit the production of nitric oxide and the activation of caspase-3/8 induced by IL-1 β and TNF- α in OA chondrocytes and reduce the production of MMP-1, MMP-3, and MMP-13 [ 89 , 90 ].…”

Therapeutic potential of alkaloids in autoimmune diseases: Promising candidates for clinical trials

“…Tg.2098 was observed as the principal peptide when inducing experimental autoimmune thyroiditis in experimental mice expressing human DRβ1‐Arg74. In addition, it inhibited T‐cell activation by thyroglobulin peptides, in particular, Tg.2098 (Li et al, 2016). Nitidine chloride induced an anti‐inflammatory effect by inhibiting TNF‐a, IL‐1b, and IL‐6 production, along with reduced NF‐kB and mitogen‐activated protein kinases (MAPK) signaling pathways in RAW264.7 cells (Wang, Jiang, Zhang, Qian, & Dua, 2012).…”