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Gene & Protein in Disease A prediction on how Epimedii herba treat periodontitis

A B

Figure 4. Protein–protein interaction (PPI) network. (A) PPI network of key targets of Epimedii herba (EH) for periodontitis. (B) PPI network of targets
screened according to the degree value, represented by node size and color depth

periodontitis were significantly higher than those in healthy
people, suggesting a positive correlation between MMP9 and
periodontitis development. The occurrence of periodontal
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inflammation is also closely associated with oxidative stress.
For instance, excessive reactive oxygen species produced by
periodontal inflammation can aggravate the inflammatory
response and activate osteoclasts, resulting in alveolar bone
resorption in patients with periodontitis. Furthermore,
MMP9, as a key gene regulating oxidative stress, can affect
the differentiation process of osteoclasts, aggravate the
inflammation of periodontal tissue, and induce the further
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absorption of periodontal supporting tissues. Another
key target, ESR1, exerted the best binding effect with
8-isopentenyl-kaempferol. Genetic polymorphisms involved
in estrogen activity may contribute to women’s susceptibility
Figure 5. Key targets of Epimedii herba (EH) for periodontitis. The top to periodontitis, and the estrogen receptor alpha gene
10 key targets based on the degree value, with darker colors representing (ESR1) PvuII and XbaI polymorphisms are associated with
greater degree value metabolic and pro-inflammatory factors in PCOS. ESR1 is
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related to the development of bone resorption, which plays
Molecular docking results showed that the active a vital role in bone metabolism, as observed in people who
components of EH had a higher −CIE value with MMP9 have bone loss after menopause or get osteopenia with ESR1
and ESR1, suggesting that they are the primary targets of EH defect. 41,42 Through multiple pathways and cytokines, ESR1
in periodontitis treatment. MMP9 is closely associated with can inhibit osteoclast differentiation and longevity, inducing
inflammation, with its expression significantly increasing the apoptosis of osteoclasts. Another possible pathway is
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in inflammatory diseases such as chronic periodontitis and that ESR1 in osteoclasts induces Fas ligand expression, which
rheumatoid arthritis. MMP9 is also a potential biomarker of in turn causes cell death through an autocrine mechanism.
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periodontitis, which can process the neutrophil chemotactic ESR1 can also inhibit the NF-κB-mediated transcription of
factor IL-8 and then improve its chemotactic effect on the IL-6 promoter by reducing the NF-κB DNA-binding
inflammatory neutrophils. In fact, it has been reported that activity, thereby regulating inflammation, immunity, and
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the levels of MMP9 in serum, GCF, and saliva of patients with stress responses. Therefore, it can be concluded that
Volume 3 Issue 4 (2024) 8 doi: 10.36922/gpd.4427