Abstract
ObjectiveTo compare the effects of transcatheter arterial chemoembolization (TACE) with transcatheter arterial embolization (TAE) on liver function, hepatic damage, and hepatic fibrogenesis in a rabbit tumor model.Materials and MethodsThirty-nine New Zealand white rabbits implanted with VX2 tumors in the left liver lobes were randomly divided into three groups: TAE, TACE, and control group. In the TAE group (n = 15), polyvinyl alcohol particles (PVAs) were used for left hepatic artery embolization. In the TACE group (n = 15), the tumors were treated with left hepatic arterial infusions of a suspension of 10-hydroxycamptothecin and lipiodol, followed by embolization with PVAs. In the control group (n = 9), the animals received sham treatment with distilled water. Serum and liver samples were collected at 6 hours, 3 days and 7 days after treatment. Liver damage was measured using a liver function test and histological analyses. Liver fibrogenesis and hepatic stellate cell (HSC) activation were evaluated using Sirius Red and anti-alpha-smooth muscle actin (α-SMA) immunohistochemical stains.ResultsTACE caused liver injury with greater increases in serum alanine aminotransferase and aspartate aminotransferase levels on day 3 (P<0.05). Histological analyses revealed increased hepatic necrosis in adjacent non-tumorous liver tissue from day 3 compared to the TAE group (Suzuki score of 2.33±1.29 versus 1.13±1.18, P = 0.001). HSC activation and proliferation were significantly increased in the TACE group compared to the control group at 3 and 7 days after treatment (0.074±0.014 vs. 0.010±0.006, and 0.088±0.023 vs. 0.017±0.009, P<0.05). Sirius Red staining demonstrated a statistically significant increase in collagen deposition in the livers in the TACE group 7 days after embolization compared to the control group (0.118±0.012 vs. 0.060±0.017, P = 0.05).ConclusionThe results of this animal study revealed that TACE induced prominent hepatocellular damage and hepatic fibrogenesis, which compromised liver function and may be responsible for chronic liver decompensation.
Highlights
Transcatheter arterial embolization (TAE) and chemoembolization (TACE) have been increasingly used as effective palliative treatments for unresectable hepatic tumors [1,2,3]
hepatic stellate cell (HSC) activation and proliferation were significantly increased in the transcatheter arterial chemoembolization (TACE) group compared to the control group at 3 and 7 days after treatment (0.07460.014 vs. 0.01060.006, and 0.08860.023 vs. 0.01760.009, P,0.05)
The results of this animal study revealed that TACE induced prominent hepatocellular damage and hepatic fibrogenesis, which compromised liver function and may be responsible for chronic liver decompensation
Summary
Transcatheter arterial embolization (TAE) and chemoembolization (TACE) have been increasingly used as effective palliative treatments for unresectable hepatic tumors [1,2,3]. TAE and TACE induce ischemic or toxic injury both in the tumors and in the adjacent hepatic tissues, which sometimes results in hepatic failure. Recent studies have suggested that the damage to normal liver parenchyma may impair the therapeutic efficacy of TAE and TACE. There has been some speculation regarding the possible causes of TAE- and TACE-induced liver damage. Liver fibrogenesis, which may be considered to be a wound healing response to liver injury, is characterized by both a quantitative increase and a qualitative change in extracellular matrix (ECM) composition. During this process, hepatic stellate cells (HSCs) are activated and proliferate, contract, induce matrix degradation, and synthesize collagen. HSC activation and liver fibrogenesis play critical roles in the homeostasis of liver repair, regeneration and fibrosis after liver injury [11,12]
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