Ganoderic acid A against cyclophosphamide‐induced hepatic toxicity in mice

Abstract

This study clarified the protective effect of ganoderic acid A (GAA) on cyclophosphamide (CP)‐induced hepatotoxicity in mice. Hepatic injury mice were induced by a single intraperitoneal injection of CP (200 mg/kg). The results showed that the levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum and liver of the CP group mice were increased, and the levels of cytokines such as interleukin (IL)‐1β, IL‐6, and tumor necrosis factor‐α in serum were increased. With the increase of the thioredoxin interaction protein (Txnip)/Trx/NF‐кB pathway, the histological structure of the liver has significantly changed as well as apoptosis events. On the contrary, the levels of ALT, AST, and cytokines in serum and liver in mice have been improved after GAA administration. Furthermore, the protein levels of the Txnip/Trx/NF‐кB pathway and apoptosis‐related protein including Bax, Bcl‐2, caspase‐3, and ‐9 were restored by GAA. In conclusion, GAA can be used as an effective drug to improve the hepatotoxicity caused by CP.

Implications of Breast Cancer Chemotherapy-Induced Inflammation on the Gut, Liver, and Central Nervous System

“…Ganglion is another potential therapeutic option for cyclophosphamide-induced liver hepatotoxicity by activating Nrf2 signaling and consequently attenuating oxidative damage, inflammation, and apoptosis in rats [126]. Ganoderic acid has also been found to attenuate hepatotoxicity by reducing cytokine levels in both serum and livers within mice [127].…”

Nerolidol protects the liver against cyclophosphamide‐induced hepatic inflammation, apoptosis, and fibrosis via modulation of Nrf2, NF‐κB p65, and caspase‐3 signaling molecules in Swiss albino mice

“…Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB p65) is speculated to be the primary mediator of hepatic inflammation that regulates the transcription of IL-6, TNF-α, IL-1β, IL-10, and transforming growth factorbeta (TGF-β). 7 Apoptosis is another decisive attribute in the CP-induced hepatotoxicity and it is manifested through oxidative stress and inflammation. 5 Therefore, oxidative stress, inflammation, and apoptosis are the three major players of CP-induced hepatotoxicity and their cumulative effect results into damaged hepatocyte membranes, leakage of hepatic enzymes into circulation and disruption of histological and ultrastructure architecture.…”

Ganoderic Acid A Inhibits Bleomycin-Induced Lung Fibrosis in Mice

“…Mice were randomly divided into 5 groups (n = 10): control group, BLM group, BLM + Dex (2 mg/kg) group, BLM + GAA (25 mg/kg), BLM + GAA (50 mg/kg). The dose of GAA was determined according to the previous studies [7,8]. Mice were anesthetized by intraperitoneal injection of pentobarbital (50 mg/kg), followed by acute intubation with intratracheal instillation of BLM (7.5 IU/kg body weight in 0.25 mL sterile PBS).…”