CQPC03 (LP-CQPC03) on preventing thrombus formation and reducing intestinal oxidative stress and inflammation in a carrageenan-induced mouse thrombosis model. High-throughput 16S rRNA sequencing determined the composition of intestinal microorganisms. Biochemical reagents, section observations, and quantitative polymerase chain reaction (qPCR) identified mouse serum and tissue-related markers. Experimental findings show that LP-CQPC03 enhances activated partial thromboplastin time (APTT) and decreases thrombin time (TT), fibrinogen (FIB), and prothrombin time (PT). LP-CQPC03 also significantly reduces black tail severity in thrombotic mice. Moreover, LP-CQPC03 lowers malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), nuclear factor kappa-B (NF-κB), and interleukin-1 beta (IL-1β) levels in thrombotic mouse serum, while increasing superoxide dismutase (SOD) and catalase (CAT) activities. Hematoxylin and eosin (H&E) pathological analysis reveals that LP-CQPC03 lessens tissue damage caused by tail vein thrombosis. In the colon tissues of thrombotic mice, LP-CQPC03 up-regulates the mRNA expression of copper/zinc superoxide dismutase (Cu/Zn-SOD), manganese superoxide dismutase (Mn-SOD), and CAT, while down-regulating NF-κB p65, IL-6, TNF-α, and interferon gamma (IFN-γ). In tail vein vascular tissues, LP-CQPC03 also suppresses the mRNA expression of NF-κB p65, intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin. Gut microbiota sequencing results show that LP-CQPC03 increases the population of beneficial bacteria and decreases harmful ones. These findings demonstrate that LP-CQPC03 prevents thrombosis in mice, reduces oxidative stress and intestinal inflammation, and regulates gut microbiota by increasing beneficial bacteria. A high concentration of LP-CQPC03 shows a better effect, comparable to heparin.
Zhao et al. (Fri,) studied this question.