Isoniazid and Rifampicin Produce Hepatic Fibrosis through an Oxidative Stress-Dependent Mechanism

Figure 2

INH and RMP induced HSC and collagenesis. Activation of stellate cells and increased hepatic collagenesis at different time periods after INH and RMP treatment. (a) mRNA expression of Col1A1 in the liver at different time points (4-24 weeks) of INH and RMP treatment. (b) Hepatic hydroxyproline content of INH and RMP-treated mice at different time periods. White bars are for control while black bars are for INH+RMP-treated mice. (c) Confocal laser scanning fluorescence microscopy of α-SMA demonstrates the localization of activated HSCs in a mouse liver. Magnification: 40x. (d) The numbers of activated HSCs as identified by the immunohistochemistry of α-SMA from the paraffin sections of the liver tissues are shown graphically. is the control, and is the INH+RMP-treated mouse. (e) mRNA expression of α-SMA in the liver at 4, 12, and 24 weeks of INH and RMP treatment. The results are expressed as the of 8 mice per group. ( versus the vehicle-treated control group; ^# versus INH and RMP-treated mice for 4 weeks; ^‡ versus INH and RMP-treated mice for 4 and 12 weeks in (a), (b), (d), and (e)).

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