thioacetamide and icariin

thioacetamide has been researched along with icariin* in 3 studies

Other Studies

3 other study(ies) available for thioacetamide and icariin

ArticleYear
Icariin attenuates thioacetamide‑induced bone loss via the RANKL‑p38/ERK‑NFAT signaling pathway.
    Molecular medicine reports, 2022, Volume: 25, Issue:4

    Topics: Alkaline Phosphatase; Animals; Body Weight; Bone Resorption; Calcium; Cell Differentiation; Collagen Type I; Disease Models, Animal; Femur; Flavonoids; Magnesium; Male; MAP Kinase Signaling System; Osteoclasts; p38 Mitogen-Activated Protein Kinases; Peptides; Phosphorus; Protective Agents; RANK Ligand; Rats, Sprague-Dawley; Thioacetamide; Transcription Factors; X-Ray Microtomography

2022
[Icariin inhibits thioacetamide-induced osteoclast differentiation through RANKL-p38/ERK-NFAT pathway].
    Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica, 2022, Volume: 47, Issue:21

    This study aims to investigate the therapeutic effect of icariin(ICA) on thioacetamide(TAA)-induced femoral osteolysis in rats. RAW264.7 cells were treated with TAA and ICA. Cell counting kit-8(CCK-8) assay was used to detect cell proliferation, and tartrate-resistant acid phosphatase(TRAP) staining to examine the formation of osteoclasts. The expression of TRAP, cathepsin K, c-FOS, and NFATc1 in RAW264.7 cells was determined by Western blot and immunofluorescence method. Thirty-two SD rats were randomized into the control group, TAA group(intraperitoneal injection of TAA at 300 mg·kg~(-1)), ICA group(gavage of ICA at 600 mg·kg~(-1)) and TAA + ICA group(intraperitoneal injection of TAA at 300 mg·kg~(-1) and gavage of ICA at 600 mg·kg~(-1)). Administration was performed every other day for 6 weeks. Body weight and length of femur were recorded at execution. Pathological injury and osteoclast differentiation of femur were observed based on hematoxylin-eosin(HE) staining and TRAP staining, and the changes of bone metabolism-related indexes alkaline phosphatase(ALP), calcium(Ca), phosphorus(P), magnesium(Mg), and cross-linked N-telopeptide of type Ⅰ collagen(NTX-Ⅰ) in serum were detected. Three-point bending test and micro-CT were applied to evaluate the quality of femur, and Western blot to detect the levels of osteoclast-related proteins TRAP, cathepsin K, RANK, RANKL, p38, p-p38, ERK, p-ERK, JNK, p-JNK, c-Fos, and NFATc1. The results showed ICA could inhibit TAA-induced production of TRAP-positive cells, the expression of osteoclast-related proteins, and nuclear translocation of NFATc1. ICA alleviated the weight loss, reduction of femur length, and growth inhibition induced by TAA in SD rats. ICA ameliorated the decline of femur elastic modulus caused by TAA and significantly restored trabecular bone mineral density(BMD), trabecular pattern factor(Tb.Pf), trabecular number(Tb.N), trabecular thickness(Tb.Th), and structure model index(SMI), thus improving bone structure. Western blot results showed ICA suppressed femoral osteoclast differentiation induced by TAA through RANKL-p38/ERK-NFATc1 signaling pathway. ICA inhibits osteoclast differentiation and prevents TAA-induced osteolysis by down-regulating RANKL-p38/ERK-NFAT signaling pathway.

    Topics: Animals; Bone Resorption; Cathepsin K; Cell Differentiation; NFATC Transcription Factors; Osteoclasts; Osteolysis; Rats; Rats, Sprague-Dawley; Thioacetamide

2022
Icariin protects against thioacetamide-induced liver fibrosis in rats: Implication of anti-angiogenic and anti-autophagic properties.
    Pharmacological reports : PR, 2017, Volume: 69, Issue:4

    Liver fibrosis is a major health problem. The current study evaluated the potential of icariin (ICA) to guard against thioacetamide (TAA)-induced liver fibrosis in rats.. Four groups of male rats were treated as follows: group 1 was the control group, group 2 was given TAA (200mg/kg), group 3 was administered ICA (50mg/kg) and TAA (200mg/kg), and group 4 was given ICA (50mg/kg) alone. Animal treatment was continued for four weeks.. Co-administration of ICA guarded against TAA hepatotoxicity as indicated by significant inhibition in the rise of serum ALT and AST activities and albumin concentrations. This was accompanied by inhibition of reduced glutathione depletion, superoxide dismutase exhaustion, and lipid peroxide accumulation. In addition, ICA inhibited the pathological alterations in liver architecture induced by TAA. The antifibrotic activity of ICA was verified by reduced hepatic collagen deposition in liver sections stained with Masson's trichrome and hepatic Col-1α mRNA and hydroxyproline contents compared to the TAA-treated group. The antiangiogenic activity of ICA was evidenced by lowered levels of mRNA of Ang-1 and protein expression of VEGF, PDGF-β, and CTGF immunohistochemically. Further, the anti-autophagic property of ICA was evidenced by amelioration of the decrease in mTOR and p70S6 kinase expression and an increase in TLR4, NFκB, IL1-β, and COX-2 immunohistochemically. Moreover, ICA antagonized the increase in HMGB1, TGF-β, and Beclin-1 and the decrease in BAMBI hepatic mRNA levels.. ICA inhibits TAA-induced liver fibrosis in rats, possibly via inhibition of angiogenesis and autophagy.

    Topics: Angiogenesis Inhibitors; Animals; Autophagy; Biomarkers; Flavonoids; Liver Cirrhosis; Neovascularization, Pathologic; Rats; Thioacetamide

2017