Insights & Discussion
The research unveils luteolin, quercetin, and kaempferol in RALRG as promising complementary components for RP treatment, with a key role in managing oxidative stress and PI3K/AKT signaling pathways.
The research used various databases such as Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform, GeneCards, and the Online Mendelian Inheritance in Man database to gather the ingredients of RALRG and potential targets of RP and RALRG. A protein-protein interaction network was constructed to visualize these interactions. The R program was utilized to perform functional enrichment. The researchers constructed a visual RALRG-RP-pathway pharmacology network using Cytoscape 3.9.1 and applied molecular docking to compute binding affinity.
The research revealed a total of 132 effective active elements in RALRG correlating to 248 target genes. Ninety-two intersection target genes were discovered from the overlap of RP- and RALRG-related genes. These intersection targets were discovered to be primarily involved in oxidative stress, responding to metal ions, and handling chemical stress. Several molecular pathways such as PI3K-AKT and MAPK were identified as closely connected to RP therapy. A potential pharmacology network was designed for the RALRG-RP-pathway with AKT1 and JUN being considered the main targets. The active ingredients luteolin, quercetin, and kaempferol were highlighted as crucial for this mechanism. RALRG overall was established as a main regulator for oxidative stress and PI3K/AKT signaling pathways in the treatment of RP.
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The team carried out both in vivo and in vitro studies. Initially, mouse retinal ganglion cells were categorized into groups based on the doses of Lycium barbarum polysaccharide they were given and a positive drug control group. These cells were then subject to different H2O2 concentrations to induce apoptosis. Techniques such as flow cytometry, immunofluorescence, and western blot were used to evaluate cell viability, apoptosis rate, and expression of various markers. For in vivo research, the team used C57/BL6 and Rd10 mice divided into similar groups as the in vitro experiment. The mice underwent drug treatment for four weeks, after which their retina's response to light and general health were evaluated using an electroretinogram and histopathological examination.
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