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- W4313334052 abstract "•Liver fibrosis is a major health problem that may progress to cirrhosis and cancer.•Cholestatic liver injury is one of the most important factors for liver fibrosis.•Lactoferrin showed a role in the treatment of bile duct ligation-induced liver fibrosis.•The anti-inflammatory action of lactoferrin might share a part in the treatment.•The treatment by lactoferrin may be via attenuating transforming growth factor-beta1/Smad2/α-SMA signaling pathway. BackgroundHepatic fibrosis is a major health issue that might lead to hepatic cirrhosis and cancer. One of its main causes is cholestasis, which has been stimulated by bile duct ligation (BDL) to block the bile flow from the liver. As for the treatment, lactoferrin (LF), the iron-binding glycoprotein, has been evaluated in various studies for the treatment of infections, inflammation, and cancer. The current study aims to investigate the curative effects of LF on BDL-induced hepatic fibrosis in rats.MethodsRats were randomly allocated into 4 groups: (1) Control sham, (2) BDL: that have been subjected to a surgery of BDL, (3) BDL + LF: 14 days later after surgery; they have been subjected to LF treatment (300 mg/kg/day, po) for two weeks, and (4) LF group has been administered (300 mg/kg/day, po) for two weeks.ResultsBDL elevated inflammatory markers (tumor necrosis factor-alpha and interleukin -1beta (IL-1β) by 635% and 250% (P ≤ 0.05), respectively, as sham group), beside it decreased the anti-inflammatory cytokine, interleukin- 10 (IL-10) by 47.7% (P ≤ 0.05) as sham group, causing inflammation, and fibrosis of the liver by the up-regulation of transforming growth factor-beta 1 (TGF-β1)/Smad2/α-smooth muscle actin (SMA) signaling pathway. LF treatment ameliorated these effects through its anti-inflammatory action (it significantly decreased tumor necrosis factor-alpha and IL-1β by 166% and 159% (P ≤ 0.05), respectively, as sham group, while increased IL-10 by 86.8% (P ≤ 0.05), as sham group) and anti-fibrotic effect by the down-regulation of TGF-β1/Smad2/α-SMA signaling pathway. These results were confirmed by histopathological examination.Conclusionlactoferrin shows promising results for the treatment of hepatic fibrosis via attenuating the TGF-β1/Smad2/α-SMA pathway and through its properties. Hepatic fibrosis is a major health issue that might lead to hepatic cirrhosis and cancer. One of its main causes is cholestasis, which has been stimulated by bile duct ligation (BDL) to block the bile flow from the liver. As for the treatment, lactoferrin (LF), the iron-binding glycoprotein, has been evaluated in various studies for the treatment of infections, inflammation, and cancer. The current study aims to investigate the curative effects of LF on BDL-induced hepatic fibrosis in rats. Rats were randomly allocated into 4 groups: (1) Control sham, (2) BDL: that have been subjected to a surgery of BDL, (3) BDL + LF: 14 days later after surgery; they have been subjected to LF treatment (300 mg/kg/day, po) for two weeks, and (4) LF group has been administered (300 mg/kg/day, po) for two weeks. BDL elevated inflammatory markers (tumor necrosis factor-alpha and interleukin -1beta (IL-1β) by 635% and 250% (P ≤ 0.05), respectively, as sham group), beside it decreased the anti-inflammatory cytokine, interleukin- 10 (IL-10) by 47.7% (P ≤ 0.05) as sham group, causing inflammation, and fibrosis of the liver by the up-regulation of transforming growth factor-beta 1 (TGF-β1)/Smad2/α-smooth muscle actin (SMA) signaling pathway. LF treatment ameliorated these effects through its anti-inflammatory action (it significantly decreased tumor necrosis factor-alpha and IL-1β by 166% and 159% (P ≤ 0.05), respectively, as sham group, while increased IL-10 by 86.8% (P ≤ 0.05), as sham group) and anti-fibrotic effect by the down-regulation of TGF-β1/Smad2/α-SMA signaling pathway. These results were confirmed by histopathological examination. lactoferrin shows promising results for the treatment of hepatic fibrosis via attenuating the TGF-β1/Smad2/α-SMA pathway and through its properties." @default.
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- W4313334052 date "2023-05-01" @default.
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- W4313334052 title "Role of Lactoferrin in Treatment of Bile Duct Ligation-Induced Hepatic Fibrosis in Rats: Impact on Inflammation and TGF-β1/Smad2/α SMA Signaling Pathway" @default.
- W4313334052 cites W1499536588 @default.
- W4313334052 cites W1506043065 @default.
- W4313334052 cites W1591767079 @default.
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- W4313334052 cites W1883333379 @default.
- W4313334052 cites W1986759094 @default.
- W4313334052 cites W1990070492 @default.
- W4313334052 cites W1990993250 @default.
- W4313334052 cites W2010106434 @default.
- W4313334052 cites W2010979263 @default.
- W4313334052 cites W2017020557 @default.
- W4313334052 cites W2035267435 @default.
- W4313334052 cites W2039245829 @default.
- W4313334052 cites W2057576662 @default.
- W4313334052 cites W2061772185 @default.
- W4313334052 cites W2066453023 @default.
- W4313334052 cites W2071649876 @default.
- W4313334052 cites W2074090345 @default.
- W4313334052 cites W2083444193 @default.
- W4313334052 cites W2100193879 @default.
- W4313334052 cites W2102018988 @default.
- W4313334052 cites W2107277218 @default.
- W4313334052 cites W2109342699 @default.
- W4313334052 cites W2114667085 @default.
- W4313334052 cites W2120858735 @default.
- W4313334052 cites W2150336290 @default.
- W4313334052 cites W2153174384 @default.
- W4313334052 cites W2192080449 @default.
- W4313334052 cites W2400754861 @default.
- W4313334052 cites W2460223128 @default.
- W4313334052 cites W2734346062 @default.
- W4313334052 cites W2771479838 @default.
- W4313334052 cites W2794330007 @default.
- W4313334052 cites W2834196515 @default.
- W4313334052 cites W2886036633 @default.
- W4313334052 cites W2886268494 @default.
- W4313334052 cites W2933110746 @default.
- W4313334052 cites W2955515366 @default.
- W4313334052 cites W2964502742 @default.
- W4313334052 cites W2969236948 @default.
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- W4313334052 doi "https://doi.org/10.1016/j.jceh.2022.12.014" @default.
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