Objective: This study was conducted to evaluate the acute and subchronic toxicity of anthraquinone. An acute toxicity test was performed in female Sprague Dawley (SD) rats, and the oral median lethal dose (LD₅₀) of anthraquinone was estimated to be >5000 mg/kg body weight (BW). In the subchronic study, groups of 10 male and 10 female rats were dosed with anthraquinone by gavage at 0, 1.36, 5.44, 21.76, and 174.08 mg/kg BW, 7 days/week for 90 days followed by a recovery period of 28 days. No appreciable toxic-related changes were observed in the 1.36 mg/kg BW group. When the animals received 5.44 mg/kg BW or more of anthraquinone, hyaline droplet accumulation in the renal tubules was observed in both the male and female rats, and anemia was observed in the females. When the anthraquinone dose reached 174.08 mg/kg BW, mild hepatocellular hypertrophy around the central vein of the hepatic lobule and hypothyroidism were observed in the female rats. During the recovery period, changes in clinical symptoms and parameters were considerably alleviated. Based on the results of this study, the no observed adverse effect level (NOAEL) for anthraquinone in rats was set at 1.36 mg/kg BW, and the lowest observed adverse effect level (LOAEL) was 5.44 mg/kg BW.

Background. Shi-Wei-Gan-Ning-San (SWGNS) is a classic Tibetan prescription, which has obvious clinical effects in the treatment of viral hepatitis, fatty liver, liver fibrosis, liver cirrhosis, liver cancer, and other liver injuries. However, animal studies and mechanism studies are still lacking. This study aimed to investigate its hepatoprotective efficacy and pharmacological mechanism in animal experiments. Methods. Chronic liver injury was induced by oral administration of carbon tetrachloride (CCl₄) in Wistar rats for 13 weeks. SWGNS was administered orally to rats at doses of 235, 705, and 1410mg/kg for 13 weeks. Blood samples were collected for biochemical, ELISA, and radioimmunoassay. Livers were harvested for H&E and immunohistochemical staining. The major constituents of SWGNS were analyzed by HPLC. In vitro experiments were used to explore the protective effect of Crocin on BRL-3A in the environment of H₂O₂. Results. SWGNS reversed weight loss is induced by CCl₄. Serum assays showed that SWGNS reduced CCl₄-induced alanine aminotransferase, aspartate aminotransferase, total bilirubin, and γ-glutamyltransferase levels and increased the total protein and albumin levels. Histopathological evaluation showed that SWGNS alleviated hepatic steatosis, fibrosis, and inflammation. Furthermore, SWNGS reduced CCl₄-induced elevations of TGF-β1, hyaluronic acid, laminin, and collagen IV in serum and reduced the high expression of α-SMA in tissues. Moreover, Crocin I and II are the main components of SWGNS. Crocin attenuated the damaging effects of H₂O₂ on BRL-3A. Conclusions. In conclusion, SWGNS alleviated CCl₄-induced chronic liver injury by inhibiting the TGF-β1 pathway. This plays an important role in promoting traditional Tibetan medicine in clinical practice.

This study systematically evaluated the toxicological safety of superoxide dismutase (SOD) as a novel food ingredient. Acute oral toxicity testing revealed no toxicity or mortality in mice of both sexes following a single gavage dose of 10 g/kg BW, classifying SOD as a practically nontoxic substance. In the 90‐day subchronic toxicity study, Wistar rats orally administered doses of 8.33, 25, or 75 mg/kg BW/day exhibited the following: Female rats in the high‐dose group showed significantly increased body weight during Weeks 11–13, transient fluctuations in food efficiency occurred in the low‐dose group, and high‐dose males displayed reduced neutrophil percentage (NEUT%) at termination, whereas all observed alterations in hematological, clinical chemistry, and urinalysis parameters lacked dose dependency and were largely disappeared during the recovery period. Histopathological examination revealed no substance‐specific lesions. Teratogenicity testing demonstrated a significant increase in fetal resorption rates in the 8.33 and 25 mg/kg BW groups ( p < 0.01), whereas this effect showed no dose–response association and no structural malformations were observed. Three genotoxicity assays (mammalian erythrocyte micronucleus, chromosome aberration in vitro, and Ames tests) yielded negative results. Collectively, these findings demonstrate a favorable safety profile for SOD at the tested doses, with no evidence of genotoxicity either in vivo or in vitro.