The Potential Hepatoprotective Effect of Paeoniae Radix Alba in Thioacetamide-Induced Acute Liver Injury in Rats

Abstract

Aim. Acute liver injury (ALI) can occur for various reasons by induced inflammation and apoptosis of liver cells including hepatocytes, Kupffer cells, and hepatic stellate cells. Thioacetamide (TAA), which is a classic hepatotoxin, causes oxidative stress, membrane damage, and accumulation of lipid droplets and subsequently provokes consecutive liver injury. In the current study, we tested whether Paeoniae Radix Alba (PR) could alleviate TAA-induced ALI. Methods. Thirty-five male rats were equally separated into five groups. The first group was the normal group, which received distilled water only. The remaining four groups received intraperitoneal TAA (200 mg/kg) for 3 days to induce ALI. The four groups were divided into the control group (no treatment), silymarin-treated, 100 mg/kg PR-treated, and 200 mg/kg PR-treated. The efficacy of PR against hepatotoxicity was evaluated in terms of the serum biochemical index and protein expression associated with inflammation and apoptosis. Moreover, the dissected livers were analyzed by hematoxylin and eosin stain. Results. PR alleviated liver dysfunction as evidenced by decreased levels of aspartate aminotransferase, alanine aminotransferase, and ammonia. Phosphorylated AMP-activated protein kinase (AMPK) and Sirtuin 1 (Sirt1) levels were obviously decreased in the TAA control group, whereas PR reversed these changes. PR also prevented deteriorative effects through inhibition of inflammation and apoptosis via nuclear transcription factor-kappa Bp65 (NF-κBp65) inactivation. Moreover, we found that the hepatoprotective effect of PR pretreatment was mediated by restoration of histopathological changes. Conclusion. PR efficiently blocked both the inflammatory response and apoptosis through activating the AMPK/Sirt1/NF-κBp65 pathway. Therefore, PR is considered a potential therapeutic agent against ALI.

Researching the molecular mechanisms of Taohong Siwu Decoction in the treatment of varicocele-associated male infertility using network pharmacology and molecular docking: A review

“…[12,13] PRA plays a powerful anti-inflammatory role by regulating the body's immune process, reducing the development of rheumatoid arthritis, liver fibrosis, and asthma. [14][15][16][17] Combining previous studies, we speculate that PS, CF, and PRA play major roles in THSWD. 782 targets related to the candidate components were obtained from the DrugBank and Swiss Target Prediction databases.…”

“…[12,13] PRA plays a powerful anti-inflammatory role by regulating the body’s immune process, reducing the development of rheumatoid arthritis, liver fibrosis, and asthma. [14–17] Combining previous studies, we speculate that PS, CF, and PRA play major roles in THSWD.…”

“…The composition degree values of quercetin, kaempferol, and luteolin were relatively high, indicating that they have a relatively important position in the network and may be the main active ingredient of THSWD in the treatment of varicocele-associated male infertility. The degree of 20 targets were above average, which were PTGS2 (46), PTGS1 (26), EGFR (24), AR (23), AKT1 (22), PARP1 (20), ESR2 (18), ESR1 (16), CASP3 (15), BCL2 (15), ACE (13), PIK3CA (13), MMP9 (13), NOS2 (12), IL6 (12), VEGFA (12), TNF (11), SHBG (10), TP53 (9) and HSP90AA1 (9) (Fig. 5B).…”

Effect of Empagliflozin on Thioacetamide-Induced Liver Injury in Rats: Role of AMPK/SIRT-1/HIF-1α Pathway in Halting Liver Fibrosis

“…Sirtuin 1 (SIRT1), in particular, controls a variety of processes during oxidative stress, including metabolism, mitochondrial function, inflammation, and apoptosis. Reduced Sirt1 expression, in turn, exacerbates the loss of AMPK, causes an inflammatory response, including the transcription of NF-κB, and increases the formation of reactive oxygen species [ 47 ]. Also, Ruderman et al said in a prior review that AMPK and SIRT-1 regulate each other and have several target molecules in common.…”

Validation of the Anticolitis Efficacy of the Jian-Wei-Yu-Yang Formula

“…Moreover, oral drug administration exacerbates the metabolic burden in the liver, which might result in metabolic disturbances and thereby increasing the susceptibility to carcinogenesis [ 86 ]. Issues regarding hepatotoxicity have been resolved by the promoted liver regeneration by BT [ 87 ], PP [ 88 ], BD [ 89 ], CH [ 90 , 91 ], LC [ 92 , 93 ], SK [ 94 ], and CWT [ 95 ]. ③ IBD patients are susceptible to malnutrition including anemia, amino acid, and vitamin deficiency [ 96 ], which could be rescued by PP [ 97 ] due to its hematopoiesis-promoting effect [ 98 – 100 ] and by the addition of pearl that is produced from shellfish mollusks which contain 20 amino acids and Fe and Mg elements [ 101 ].…”