1. The Ameliorative Effects of Saikosaponin in Thioacetamide-Induced Liver Injury and Non-Alcoholic Fatty Liver Disease in Mice
Geng-Ruei Chang, Wei-Li Lin, Tzu-Chun Lin, Huei-Jyuan Liao, Yu-Wen Lu Int J Mol Sci. 2021 Oct 21;22(21):11383. doi: 10.3390/ijms222111383.
Liver disorders are a major health concern. Saikosaponin-d (SSd) is an effective active ingredient extracted from Bupleurum falcatum, a traditional Chinese medicinal plant, with anti-inflammatory and antioxidant properties. However, its hepatoprotective properties and underlying mechanisms are unknown. We investigated the effects and underlying mechanisms of SSd treatment for thioacetamide (TAA)-induced liver injury and high-fat-diet (HFD)-induced non-alcoholic fatty liver disease (NAFLD) in male C57BL/6 mice. The SSd group showed significantly higher food intake, body weight, and hepatic antioxidative enzymes (catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD)) and lower hepatic cyclooxygenase-2 (COX-2), serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), interleukin (IL)-1β, tumor necrosis factor (TNF)-α, and fibroblast growth factor-21 (FGF21) compared with controls, as well as reduced expression of inflammation-related genes (nuclear factor kappa B (NF-κB) and inducible nitric oxide synthase (iNOS)) messenger RNA (mRNA). In NAFLD mice, SSd reduced serum ALT, AST, triglycerides, fatty acid-binding protein 4 (FABP4) and sterol regulatory element-binding protein 1 (SREBP1) mRNA, and endoplasmic reticulum (ER)-stress-related proteins (phosphorylated eukaryotic initiation factor 2α subunit (p-eIF2α), activating transcription factor 4 (ATF4), and C/EBP homologous protein (CHOP). SSd has a hepatoprotective effect in liver injury by suppressing inflammatory responses and acting as an antioxidant.
2. Biosynthesis of L-alanine, a major amino acid of fibroin in Samia cynthia ricini
M Osanai, M Okudaira, J Naito, M Demura, T Asakura Insect Biochem Mol Biol. 2000 Mar;30(3):225-32. doi: 10.1016/s0965-1748(99)00120-4.
The derivation of alanine in fibroin was investigated using NMR and selective isotopic labelling. 2H2O infused orally into 5th instar larvae was incorporated into the proton of the methyl group of alanine in fibroin. Proton exchange among alanine, glycine and serine was also found. Incorporation of 13C from [2-(13)C]acetate into alanine C2 and C3 and glycine C2 in fibroin, and also C4 of free glutamine plus glutamate was observed in vivo. Hemolymph contained a peak for C4 of glutamate plus glutamine, and an alanine C3 peak appeared transiently. Thus, it is suggested that the C-skeleton of alanine formed was derived from L-malate via the TCA-cycle, and that this alanine is utilized in part for fibroin synthesis. Spectra of the hemolymph extract of larvae infused orally with [15N2]urea showed no 15N-compounds, whereas those of larvae injected subcutaneously showed only one peak of urea, whose intensity decreased with time, as shown in the in vivo spectra of a living larva infused with [15N2]urea. The solution NMR spectrum of fibroin showed no 15N-labelled compounds. Temporal changes in the peak intensities of six compounds in the spectra of a living larva infused with [15N]ammonium demonstrated a process in which 15N was incorporated into fibroin containing 15N-alanine through the amide group of glutamine and the amino group of glutamate. Thus, alanine biosynthesis from the TCA-cycle originates mainly from water, L-malate and ammonium. The fact that no 15N-urea was detected in the hemolymph extract of larvae infused with [15N]ammonium suggests that 15N-urea found in the above in vivo spectra may be that accumulated in the hindgut. Thus, excess ammonium in the body causes the production of urea by the urea-cycle. In Samia larvae, urea was not reutilized but excreted. The metabolic relationships between the assimilation of ammonium and the function of the urea-cycle are discussed.
3. The Allium triquetrum L. Leaves Mitigated Hepatotoxicity and Nephrotoxicity Induced by Lead Acetate in Wistar Rats
Labiba Kahalerras, Ines Otmani, Cherif Abdennour Biol Trace Elem Res. 2022 Nov;200(11):4733-4743. doi: 10.1007/s12011-021-03052-y. Epub 2022 Jan 2.
The aim of this study was to scrutinize the possible mitigating role of leaves' Allium triquetrum L. against the toxicity of lead acetate on liver and kidney markers of Wistar rat. Lead acetate (Pb) and leaves' aqueous extracts (L) were orally administrated for 3 weeks. Rats were divided into the control, Pb group (500 mg/kg body weight/day), positive controls L (2g, 3g, 4g/kg BW/day), along with three combined groups of the same doses (Pb-L1, Pb-L2, Pb-L3). The levels of plasma aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), total proteins (TP), albumin (ALB), urea, creatinine (Cr), and uric acid (UA), as well as the hepatic and the renal malondialdehyde (MDA), glutathione (GSH), and glutathione peroxidase (GPx), were estimated. Results exhibited a significant increase in plasma AST, ALT, ALP, urea, creatinine, uric acid, and MDA levels of the Pb group compared to the control, with the exception of TP, ALB, GSH levels, and GPx activities that were significantly diminished, though the co-administration of garlic extracts (Pb-L) revealed a significant decrease in all mentioned markers, excluding the TP, ALB, GSH, and GPx levels. Likewise, Pb caused histological injuries in the hepatic and renal tissues of rats, while the co-administration of leaves' wild garlic has reduced such effect. Thought, the Pb-L has attenuated the Pb-induced toxicity in a dose-dependent manner. In conclusion, the aqueous extracts of A. triquetrum have the potential to alleviate Pb hepatotoxicity and nephrotoxicity through the modulation of most biomarkers in Wistar rat.
