Meta-analysis of Shenqi Fuzheng Injection Combined with Chemotherapy in Treatment of Colorectal Cancer

[Objectives] To make a systematic evaluation of the clinical efficacy and safety of Shenqi Fuzheng Injection in the treatment of colorectal cancer. [Methods] Databases,such as China National Knowledge Infrastructure( CNKI),Wanfang,China biomedical literature service system( CBM),CQVIP,Medline,and Cochrane,were searched for the time before April 2017. The randomized controlled trial( RCT) that met the inclusion criteria was screened. Then,quality evaluation was made based on the modified Jadad scale. Data were extracted and meta-analysis was made with the aid of Review Manager 5. 3. [Results] Finally,21 papers met the inclusion criteria,including 2 high quality papers. The average Jadad score was 2. 5 points,1 589 patients were included. Meta-analysis results showed that the intervention of the experimental group could improve the quality of life[OR = 3. 32,95% CI( 2. 33,4. 74),P < 0. 000 01]; improve the short-term efficacy[OR =1. 68,95% CI( 1. 26,2. 24),P =0. 000 4]; reduce the incidence of adverse chemotherapy reactions such as reducing the gastrointestinal reactions[OR = 0. 33,95% CI( 0. 25,0. 43),P < 0. 000 01],reducing myelosuppressive reactions[OR = 0. 33,95% CI( 0. 24,0. 46),P < 0. 000 01]; improve the immune functions,such as increasing CD4/CD8 cell ratio[WMD = 1. 19,95% CI( 0. 24,0. 41),( P <0. 000 01) ],and increasing the number of NK cells[WMD =1. 72,95% CI( 5. 62,14. 30),( P <0. 000 01) ]. [Conclusions]The clinical effect of Shenqi Fuzheng Injection in the treatment of colorectal cancer is better than that of chemotherapy alone,but it needs more highquality RCTs to improve the level of research.

Myelin Oligodendrocyte Glycoprotein-IgG Contributes to Oligodendrocytopathy in the Presence of Complement, Distinct from Astrocytopathy Induced by AQP4-IgG

Immunoglobulin G against myelin oligodendrocyte glycoprotein(MOG-Ig G) is detectable in neuromyelitis optica spectrum disorder(NMOSD) without aquaporin-4 Ig G(AQP4-Ig G), but its pathogenicity remains unclear.In this study, we explored the pathogenic mechanisms of MOG-Ig G in vitro and in vivo and compared them with those of AQP4-Ig G. MOG-Ig G-positive serum induced complement activation and cell death in human embryonic kidney(HEK)-293 T cells transfected with human MOG. In C57 BL/6 mice and Sprague-Dawley rats, MOG-Ig G only caused lesions in the presence of complement. Interestingly, AQP4-Ig G induced astroglial damage, while MOGIg G mainly caused myelin loss. MOG-Ig G also induced astrocyte damage in mouse brains in the presence ofcomplement. Importantly, we also observed ultrastructural changes induced by MOG-Ig G and AQP4-Ig G. These findings suggest that MOG-Ig G directly mediates cell death by activating complement in vitro and producing NMOSDlike lesions in vivo. AQP4-Ig G directly targets astrocytes,while MOG-Ig G mainly damages oligodendrocytes.