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Miss Jane's Building (Edisto Library Temporary Location)
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Lupus Recipe inhibits cGVHD‐induced lupus nephritis in mice and promote renal LC3‐associated autophagy.
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- Author(s): Liu, Ruihua; Huang, Xuan; Ye, Hongjian; Wu, Haishan; Guo, Jing; Peng, Yuan; Wu, Meiju; Fan, Jinjin; Yang, Xiao
- Source:
Immunity, Inflammation & Disease; Mar2023, Vol. 11 Issue 3, p1-11, 11p- Subject Terms:
- Source:
- Additional Information
- Abstract: Lupus nephritis (LN) is one of the most severe manifestations of systemic lupus erythematosus (SLE). The chronic graft versus host disease (cGVHD) mouse model is a well‐established model of SLE. LC3‐associated autophagy plays a critical role in extracellular particle clearance, including pathogens and apoptotic cells. Lupus Recipe (LR) is a Chinese herbal compound that has been proven to be effective in treating SLE. In the study, we investigated the protective effects of LR or LR combined with prednisone on cGVHD mouse model and LC3‐associated autophagy in the kidney. The mice were subjected to six groups. The LR treatment group received LR at the dosage of 1.15 and 2.3 g/kg/day, respectively. The corticosteroid treatment group received prednisone at a dosage of 5 mg/kg/day. The combination treatment group received LR at a dosage of 2.3 g/kg/day, and prednisone at 2.5 mg/kg/day. LR treatment reduced proteinuria and serum triglyceride levels, as well as spleen weight. LR also alleviated pathologic damage and immunoglobulin G deposition in the kidney. LR combined with a low dose of prednisone significantly improved kidney function and decreased serum triglyceride, total cholesterol, and spleen weight. In addition, combination treatment relieved kidney injury more effectively than LR alone. Western blot revealed that LR treatment or LR combined with prednisone increased the LC3‐associated autophagy protein of Rubicon and Nox2, as well as LC3I levels in the kidney tissues. In conclusion, LR inhibited the manifestation of cGVHD‐induced LN, which may attribute to the increased levels of LC3‐associated autophagy. [ABSTRACT FROM AUTHOR]
- Abstract: Copyright of Immunity, Inflammation & Disease is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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