Abstract
In Uygur medicine, Huganbuzure granule (HBG) is one of the classical prescriptions for liver protection. However, its role in immune liver injury remains unknown. This study evaluates the effect of HBG on concanavalin-A- (ConA-) induced immune liver injury and investigates its protective underlying mechanism. BALB/c mice were randomly divided into five groups (n = 24 mice per group): control, ConA, 1.6 g/kg HBG + ConA, 3.2 g/kg HBG + ConA, and 6 mg/kg prednisolone + ConA. HBG was intragastrically administrated once daily for ten consecutive days, prior to ConA (20 mg/kg) injection. The levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TBIL), superoxide dismutase (SOD), and malondialdehyde (MDA) in mouse serum were measured after ConA injection. Moreover, liver-related mRNA levels were evaluated by qPCR. The detection of liver-related proteins was assessed by immunohistochemistry and western blot analysis. Compared with the ConA group, HBG reduced the mRNA expression of IL-17A and IFN-γ and the protein expression of T-bet and ROR-γt. In addition, HBG increased the mRNA expression of IL-4 and TGF-β and protein expression of GATA3 and Foxp3, indicating that HBG regulated the balance of Th1/Th2 and Th17/Treg. Furthermore, HBG alleviated immune liver injury by reducing oxidative stress, inhibiting apoptosis, and decreasing the expression of p-JNK, p-ERK, p-p38, p-JAK1, p-STAT1, p-STAT3, and IRF1. Our data suggested that HBG attenuated ConA-induced immune liver injury by regulating the immune balance and inhibiting JAK1/STATs/IRF1 signaling, thereby reducing apoptosis induced by JNK activation. The findings indicate that HBG may be a promising drug for immune liver injury.
Highlights
Immune liver injury is a progressive inflammatory disorder that is closely related to abnormal immune stimulation of liver cells, which may start with acute hepatitis that can eventually result in liver cirrhosis, liver cancer, and even death [1,2,3,4]
Our data showed that serum levels of ALT, AST, and total bilirubin (TBIL) significantly increased in the concanavalin A (ConA) group at all time points and reached a peak at 4 h (p < 0.01) (Figures 1(b)–1(d))
Treatment with Huganbuzure granule (HBG), especially, significantly reduced liver necrosis. These results showed that HBG effectively reduced ConA-induced immune liver injury in mice
Summary
Immune liver injury is a progressive inflammatory disorder that is closely related to abnormal immune stimulation of liver cells, which may start with acute hepatitis that can eventually result in liver cirrhosis, liver cancer, and even death [1,2,3,4]. It has been reported that 1 and 2 cells play an important role in immunological hepatic. As a major constituent of programmed cell death, plays an important role in ConA-induced immune liver injury [13]. In Uygur medicine, HBG is one of the classical prescriptions for liver protection. It is mainly composed of Foeniculum vulgare Mill. (Umbelliferae), Semen et radix cortex of Cichorium intybus L. E purpose of this study was to establish an immune liver injury model in mice to investigate the underlying mechanism of HBG in maintaining the homeostasis of 1/ 2 and Treg/ 17 in mice and evaluate the antiapoptosis effects HBG is widely used in the treatment of chronic liver disease [18]; the specific underlying mechanisms of HBG in liver protection have yet to be elucidated. e purpose of this study was to establish an immune liver injury model in mice to investigate the underlying mechanism of HBG in maintaining the homeostasis of 1/ 2 and Treg/ 17 in mice and evaluate the antiapoptosis effects
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: Evidence-Based Complementary and Alternative Medicine
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
