ENDOGL1 inhibitors function primarily by mitigating oxidative stress or suppressing the immune response. For instance, N-acetyl-cysteine is an antioxidant that can reduce oxidative stress. Given that ENDOGL1 is sensitive to oxidative stress, the reduction of this stress by N-acetyl-cysteine can indirectly inhibit the functional activity of ENDOGL1. Similarly, ethanol and sodium nitroprusside can increase oxidative stress, which can indirectly lead to the inhibition of ENDOGL1's functional activity.
On the other hand, certain ENDOGL1 inhibitors, such as dexamethasone and prednisone, are glucocorticoids that can suppress the immune response. Since ENDOGL1 is involved in inflammatory responses, the suppression of the immune response by these glucocorticoids can lead to the indirect inhibition of ENDOGL1's functional activity. Non-steroidal anti-inflammatory drugs like aspirin, ibuprofen, and naproxen inhibit cyclooxygenases, which canalso lead to the indirect inhibition of ENDOGL1's functional activity. Immunosuppressive drugs such as hydroxychloroquine, methotrexate, cyclosporine, and tacrolimus can reduce the immune response or disrupt T cell signaling, which can indirectly inhibit the functional activity of ENDOGL1.
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