Prolactin stimulates the proliferation of normal female cholangiocytes by differential regulation of Ca2+-dependent PKC isoforms

Table 1 Evaluation of prolactin serum levels, inflammation, necrosis, lobular damage and apoptosis in liver sections after in vivo administration of: (i) NaCl or prolactin to normal rats for 1 week; or (ii) anti-prolactin antibody or non-immune serum to BDL (immediately following BDL) rats for 1 week.

Treatment	Normal rats + NaCl for 1 week	Normal rats + PRL for 1 week	BDL rats + non-immune serum for 1 week	BDL rats + anti-PRL antibody for 1 week
Prolactin serum levels (ng/ml)	6.6 ± 0.16	98.4 ± 1.5*	63.4 ± 1.0	14.0 ± 0.2*
Inflammation	0 ± 0	0.4 ± 0.2^ns	1.6 ± 0.2	0.8 ± 0.2*
Necrosis	0 ± 0	0.42 ± 0.2^ns	1.0 ± 0.0	0.6 ± 0.2*
Lobular damage	0.06 ± 0.06	0.26 ± 0.11^ns	1.8 ± 0.14	0.9 ± 0.06*
Cholangiocyte Apoptosis	0 ± 0	0.2 ± 0.2^ns	0.6 ± 0.2	0.8 ± 0.2^ns

Inflammation, necrosis, lobular damage and apoptosis were evaluated in paraffin embedded liver sections (5 μm) stained with hematoxylin and eosin. In vivo administration of prolactin to normal rats for 1 week increased prolactin serum levels but did not alter liver inflammation, necrosis, lobular damage or apoptosis compared to NaCl-treated normal female rats. The administration of anti-prolactin antibody to BDL female rats decreased prolactin serum levels and ameliorated portal inflammation, necrosis and lobular damage compared to BDL rats treated with non-immune serum for 1 week. Data on prolactin serum levels are mean ± SEM of 3 samples from 3 different rats. Data (mean ± SEM) related to the measurement of inflammation, necrosis, lobular damage and cholangiocyte apoptosis are obtained from the analysis of 3 slides per portal tract. *p < 0.05 vs. its corresponding value from BDL rats treated with non-immune serum.

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