5 It offers a standardized way of preparing reports of trial findings that facilitates accurate and transparent reporting with critical appraisal and interpretation. More and more highly cited academic journals, including HEPATOLOGY, have adopted the CONSORT statement for standardization and integrity. In China, CONSORT for TCM has been
developed and widely adopted; it provides more specificity and sensitivity for the assessment of TCM methodological quality.6 Therefore, it would have been much better if the CONSORT standard, instead of GSI-IX price Jadad scoring, had been used in this meta-analysis. In summary, the methodological quality of the analysis needs to be reassessed. Ming-Hua Zheng M.D.*, Yu-Chen Fan M.D., Ke-Qing Shi M.D.*, Yong-Ping Chen M.D.*, * Liver Research Center, Department of Infection and Liver Diseases, First
Affiliated Hospital, Wenzhou Medical College, Wenzhou, China, Department of Hepatology, Qilu Hospital, Shandong University, Jinan, China. “
“We read the article by Horiguchi et Metformin al.1 with great interest. It is a commonly accepted dogma that inflammation induces necrosis and apoptosis of hepatocytes during liver damage. However, clinicians have found that inflammation does not always correlate with hepatocellular damage in chronic liver disease. How to explain the conflict? By using a well-established model of mice with specific deletion of signal transducer and activator of transcription 3 in myeloid cells (STAT3mye−/−), Horiguchi and colleagues surprisingly found more inflammatory cells, eg, neutrophils, but less necrosis/apoptosis in the liver of STAT3mye−/− mice than in wild-type mice after carbon tetrachloride (CCl4) treatment. STAT3mye−/− mice had higher hepatic STAT3 activation and became resistant to hepatic oxidative stress after CCl4 injection compared with wild-type
mice. In contrast to STAT3mye−/− mice, hepatocyte-specific STAT3 knockout (STAT3Hep−/−) mice had more liver necrosis/apoptosis but less inflammation after CCl4 treatment compared with wild-type mice. An additional Immune system deletion of hepatocyte STAT3 in STAT3mye−/− mice restored CCl4-induced hepatic necrosis but reduced liver inflammation. This study suggests that inflammation associated with a predominance of hepatoprotective cytokines may reduce rather than accelerate hepatocellular damage via activation of hepatocyte STAT3 in CCl4-induced liver damage. The data elucidate a potential mechanism that inflammation does not always correlate with hepatocellular damage. Interestingly, the same group had also previously investigated inflammation and hepatocellular damage in the same strain of STAT3mye−/− mice treated with concanavalin A (ConA) or ethanol.