Background: Neuroinflammation and oxidative stress are critical players in intracerebral hemorrhage (ICH). Geniposide is an active component of Gardenia that has anti-inflammatory effects. This study focused on the roles and mechanisms of geniposide in ICH.
Methods: ICH was established by injecting collagenase IV into C57BL/6 mice. To determine the functions of geniposide and NF-κB inhibition in ICH model mice, geniposide (1, 25, or 50 mg/kg) or PDTC (a NF-κB inhibitor) was administered. Neurological functions were assessed with the modified neurological severity score (mNSS) test. Hematoxylin and eosin staining were performed to identify pathological changes. IL-1β and TNF-α levels were estimated with ELISA kits. NF-κB p65 localization was determined by immunofluorescence staining. Oxidative stress was analyzed by measuring ROS levels.
Results: Geniposide alleviated cerebral edema and neurological deficits. Geniposide inhibited neuroinflammation and oxidative stress after ICH, and the inhibitory effects were enhanced by NF-κB inhibition. Additionally, geniposide inhibited NF-κB signaling.
Conclusion: Geniposide alleviates brain injury by suppressing inflammation and oxidative stress damage in experimental ICH models by inhibiting NF-κB signaling.
Keywords: Intracerebral hemorrhage; NF-κB; geniposide; inflammation; oxidative damage.