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Nardostachys jatamansi (Spikenard) and Ocimum tenuiflorum (Holy Basil)
Published in Azamal Husen, Herbs, Shrubs, and Trees of Potential Medicinal Benefits, 2022
Mani Iyer Prasanth, Premrutai Thitilertdecha, Dicson Sheeja Malar, Tewin Tencomnao, Anchalee Prasansuklab, James Michael Brimson
The ethanolic extract of N. jatamansi rhizomes are hepatoprotective against thioacetamide-induced hepatotoxicity in rats (200 mg/kg body wt.). Oral administration of a 50% solution of the N. jatamansi ethanol extract (800 mg/kg body wt.) over three days before thioacetamide treatment resulted in a significant increase in the survival of the rats (approximately 20–75%). Furthermore, there was an improvement in serum transaminases (aminotransferases) and alkaline phosphatase in the N. jatamansi cotreated rats (Ali et al., 2000). A separate study evaluated the effect of Nardostachys jatamansi on liver damage caused by ionizing irradiation. N. jatamansi mediated reduction in serum bilirubin levels, glutamic oxallotransaminase, and serum pyruvic oxallotransaminase levels in the blood of rats treated with 200 mg/kg body wt. N. jatamansi before whole-body radiation at a dose of 3Gy (Ali et al., 2000).
Biochemical Aspects of Fatty Liver
Published in Robert G. Meeks, Steadman D. Harrison, Richard J. Bull, Hepatotoxicology, 2020
Thioacetamide is another poison producing centrolobular fat infiltration and cell death (Barker et al., 1963; Thoënes and Bannasch, 1962). It provokes heavy nucleolar damage, as well as impairment in both RNA synthesis and release to the cytoplasm (Smuckler and Koplitz, 1974). The large (50 S) ribosomal subunits have been found to be intensively phosphorylated, but the mechanism for this is still not understood (Gressner and Greiling, 1978). Mitochondrial damage has been also described (Muller and Dargel, 1984).
Heterotopic Auxiliary Liver Transplantation in Rats
Published in Waldemar L. Olszewski, CRC Handbook of Microsurgery, 2019
Thioacetamide cirrhosis (TAA) was chosen as a model for chronic liver damage. Depending on dosage and time span of application, a cirrhosis of the small-to-large nodular type was produced, which histologically showed hyperplastic or hyperplastic-hypertrophic, often even hepatoma-like cells, and signs of portal hypertension (see the chapter on Microsurgery in the Portal Area of the Rat). Over a period of 4 to 5 months, the animals were given a 3% TAA solution for drinking water. The average intake ran from 4.3 to 5.5 mg TAA per day for each animal. The total amount, therefore, came to about 700 mg; 48 hr prior to the operation, the TAA was stopped, in order to avoid any toxic side effects.
WRH-2412 alleviates the progression of hepatocellular carcinoma through regulation of TGF-β/β-catenin/α-SMA pathway
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2023
Mohammed A. F. Elewa, Wagdy M. Eldehna, Ahmed M. E. Hamdan, Samraa H. Abd El-kawi, Asmaa M. El-Kalaawy, Taghreed A. Majrashi, Reham F. Barghash, Hatem A. Abdel-Aziz, Khalid S. Hashem, Mohammed M. H. Al-Gayyar
The animal protocol was approved by Institutional Animal Care and Use Committee, Beni-Suef University (BSU-IACUC), Approval number: 022–347. Forty Sprague–Dawley adult male rats weighing 180–200 g were used. All animals were kept under standard conditions of temperature (25 °C) with a regular 12 h light/12 h dark cycle. Each animal was examined daily and weighed weekly throughout the 16 weeks experiential period. They were classified randomly into five groups, each consisted of 10 rats.Control group: Rats recieved intraperitoneal (i.p.) injection of phosphate buffer saline (PBS, 10 mM, pH 7.4) twice weekly for 16 weeks.WRH-2412-treated control group: Rats were injected with 5 mg/kg i.p. WRH-2412 twice weekly for 16 weeks.HCC group: Rats were i.p. injected with 200 mg/kg thioacetamide (TAA; Tocris Bioscience) twice weekly for 16 weeks.HCC treated with WRH-2412: Rats were i.p. injected with 5 mg/kg WRH-2412 twice weekly for 16 weeks accompanied by 200 mg/kg TAA i.p., twice weekly for 16 weeks.
Hepatoprotective Effect of Antrodia cinnamomea Mycelium in Patients with Nonalcoholic Steatohepatitis: A Randomized, Double-Blind, Placebo-Controlled Trial
Published in Journal of the American College of Nutrition, 2021
Ya-Ling Chiou, Charng-Cherng Chyau, Tsung-Ju Li, Chia-Feng Kuo, Yu-Yling Kang, Chin-Chu Chen, Wang-Sheng Ko
This six-month double-blind randomized placebo-controlled parallel study was performed in adult human subjects with NASH. Participants were treated with three capsules per day containing either 420 mg of ACM or 420 mg of starch (placebo) with similar appearance and taste. The basis of the ACM dose was based on the same material applied on other in vivo study (18) which indicated that the dose of 131 mg/Kg in rat is equivalent to 1456 mg/day for human presents significantly protective effects against the thioacetamide-induced liver fibrosis. Both groups received standardized lifestyle modification. The participants were required to follow a predetermined regular visit to Kuang Tein General Hospital every three months during the intervention period (6 months). During each study visit, subjects underwent anthropometric measurements and blood testing for biochemical analysis, immune function assay, inflammatory cytokines assay, and FibroMax test.
Molecular mechanism and research progress on pharmacology of traditional Chinese medicine in liver injury
Published in Pharmaceutical Biology, 2018
Hong Yang Zhang, Hong Ling Wang, Guo Yue Zhong, Ji Xiao Zhu
Thioacetamide is commonly used to induce hepatotoxicity in hepatic model. The toxic effect of TAA is attributed to its biological activity exerted through oxidase systems, particularly CYP450 2E1 and FAD monooxygenase. The bioactivation of TAA further lead to the formation of reactive metabolites (thioacetamide-S-dioxide), followed by thioacetamide sulphene and sulfone that covalently bind to cellular macromolecules or cellular membrane. Upon binding, TAA enhances oxidative stresses, and subsequently destroys the cellular integrity and initiates necrosis. TAA can be transformed into sulfone, and then to sulfoxide through the conversion of TAA-oxysulfide by CYP450 metabolizing enzymes. These metabolites suppress the phagocytosis of the monocyte to red blood cells, eliminate the capability of the endotoxin of Kupffer cells, promote endotoxemia formation, and lead to enterogenous toxicemia. Depletion of macrophages extends coagulation necrosis with elevated levels of hepatic enzymes at the early stage, which results in unsuccessful reparative fibrosis and dystrophic calcification at the end stage.