Inhibitory Effects of Corydalis saxicola Bunting Total Alkaloids on Macrophage Pyroptosis

Author:

Feng Cong12345,Yong Xiangzhi12345,Jiang Qiaozhi12345,Su Zhiheng6,Liu Zhenmin12345,Wu Tiantian15,Tao Renchuan12345

Affiliation:

1. Department of Periodontics and Oral Medicine College of Stomatology Guangxi Medical University Nanning P. R. China

2. Guangxi Health Commission Key Laboratory of Prevention and Treatment for Oral Infectious Diseases Nanning P. R. China

3. Guangxi Key Laboratory of Oral and Maxillofacial Rehabilitation and Reconstruction Guangxi Universities

4. Colleges Key Laboratory of Oral and Maxillofacial Surgery Disease Treatment Guangxi Clinical Research Center for Craniofacial Deformity Nanning P. R. China

5. Guangxi Key Laboratory of AIDS Prevention and Treatment Guangxi Medical University Nanning P. R. China

6. Pharmaceutical College Guangxi Medical University

Abstract

AbstractThis study investigated the effect of Corydalis saxicola Bunting total alkaloids (CSBTA) on pyroptosis in macrophages (Mϕ). In the Mϕ pyroptosis model, an inverted fluorescence microscope was used to assess cell pyroptosis, while a scanning electron microscope was used to observe morphological changes in Mϕ. NLR family pyrin domain‐containing 3 (NLRP3), caspase‐1, and gasdermin D (GSDMD) expression levels were detected by polymerase chain reaction and western blotting, whereas interleukin‐1 (IL‐1) and interleukin‐18 (IL‐18) expression levels were measured by an enzyme‐linked immunosorbent assay. After pretreatment with CSBTA or the caspase‐1 inhibitor, acetyl‐tyrosyl‐valyl‐alanyl‐aspartyl‐chloromethylketone (Ac‐YVAD‐cmk), it was discovered that NLRP3, caspase‐1, and GSDMD expressions were significantly reduced at both the mRNA and protein levels, as were IL‐1 and IL‐18 levels. The inhibitory effects of CSBTA and Ac‐YVAD‐cmk did not differ significantly. These findings indicate that CSBTA blocks Porphyromonas gingivalis‐lipopolysaccharide‐induced Mϕ pyroptosis.

Funder

National Natural Science Foundation of China

Publisher

Wiley

Subject

Molecular Biology,Molecular Medicine,General Chemistry,Biochemistry,General Medicine,Bioengineering

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