Taohong siwu decoction attenuates AIM2 and NLRC4 inflammasomes by ameliorates deoxyribonucleic acid damage after ischemic stroke

Abstract

Taohong siwu decoction (THSWD) has been shown to have a therapeutic effect on ischemic strokes (IS). However, it is not clear to us whether THSWD reduces deoxyribonucleic acid (DNA) damage after stroke and reduces the inflammatory response caused by the damage. Therefore, we constructed an IS model (I/R) in rats and performed oxygen-glucose deprivation/reoxygenation (OGD/R) on BV2 cells. Then ELISA, immunofluorescence staining, immunohistochemistry staining, and RT-qPCR were performed to detect the expressions of absent in melanoma 2 (AIM2), NLRC4, and Caspase-1 inflammasomes and other inflammatory factors. Experimental stroke causes DNA damage, and we found that the aforementioned inflammasomes as well as inflammatory factors were significantly inhibited after treatment with THSWD by comparing the model group with the model administration group. In addition, we examined the expression of AIM2, NLRC4, and Caspase-1 in BV2 cells of OGD/R and found that the expression of the aforementioned inflammasomes was significantly decreased in OGD/R by administration of THSWD-containing serum. Our data suggest that THSWD can reduced DNA damage after stroke as well as the inflammatory response caused by the damage.

Protective effect of Tao Hong Si Wu Decoction against inflammatory injury caused by intestinal flora disorders in an ischemic stroke mouse model

“…Previously, our group identified the five major components of THSWD (gallic acid, protocatechuic acid, hydroxysafflor yellow A, amygdalin, and paeoniflorin) with the aid of UPLC-QTOF-MS [ 17 ]. In recent years, our group has made some conclusions through in vivo and in vitro experiments that THSWD can reduce inflammatory injury and nerve injury by regulating mitochondrial DNA and nuclear DNA [ 18 ], mitochondrial autophagy and activation of NLRP3 inflammatory vesicles in ischemic stroke rats [ 19 ]. In vivo, it is also confirmed that THSWD inhibits the mitochondrial autophagy-NLRP12 inflammatory body pathway of brain cells to protect brain cells from injury [ 20 ].…”