Effect of 17beta-estradiol on phosphorylcholine cytidylyltransferase activity from cultured rat lung explants / 中国应用生理学杂志

<p><b>AIM</b>To investigate the influence and mechanisms of 17beta-estradiol on the CTP: phosphorylcholine cytidylyltransferase (CCT) activity from cultured lung explants without serum.</p><p><b>METHODS</b>We detected the amount of [M-14C] choline incorporation into phosphatidylcholine so as to reflect CCT activity by liquid scintillation.</p><p><b>RESULTS</b>(1) 17beta-estradiol increased the CCT activity in dose-dependence and time-dependence. (2) Both the protein kinase C inhibitor H-7 and calmodulin antagonist W-7 abolished the stimulatory effect of 17beta-estradiol (3 x 10(-6) mol/L) on the CCT activity.</p><p><b>CONCLUSION</b>17beta-estradiol can increase CCT activity in cultured lung explants, its mechanism is related to protein kinase C and calmodulin.</p>

Effect of sex hormones on secretion of lysozyme in alveolar macrophage / 中国应用生理学杂志

<p><b>AIM AND METHODS</b>To further explore the functions of alveolar macrophage and their modulation mechanisms, the activity of lysozyme in rat alveolar macrophage assessed by electrophoresis was determined. The effects of androsterone and estradiol on lysozyme secretion and their mechanisms were also studied.</p><p><b>RESULTS</b>The results showed that androsterone and estradiol increased activity of lysozyme significantly (P < 0.01), indomethacin abolished those effects. This suggests that the insufficiency of sex hormones secretion as the retrogression of gonads is involved in the decrease of immunological functions, and the susceptibility to infectious diseases.</p><p><b>CONCLUSION</b>Sex hormones increased activity of lysozyme, and those effects related to prostaglandin.</p>

Protective effect of low concentration endothelin-1 on the reactive oxygen-induced inhibition of pulmonary surfactant lipid synthesis / 生理学报

The effects of endothelin-1 (ET-1) at low concentration (1-100 pmol/L) on the reactive oxygen-induced inhibition of both pulmonary surfactant (PS) lipid synthesis and the activity of CTP: phosphorylcholine cytidylyltransferase (CCT), a rate-limiting enzyme in biosynthesis of phosphoatidylcholine (PC), were studied in cultured lung explants without serum. The xanthine-xanthine oxidase superoxide anion generating system decreased (3)H-choline incorporation into PC in a dose-dependent manner in cultured lung explants. ET-1 reduced both the reactive oxygen-induced decrease in (3)H-choline incorporation and the increase in malondialdehyde (MDA) content of lung tissues, but did not change the levels of antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) and the total antioxidant capability in the lung explants. ET-1 enhanced microsomal CCT activity of the lung tissues, while it decreased cytosolic CCT activity of lung tissues. ET-1 also prevented the inhibitive effect of reactive oxygen on microsomal CCT activity in the lung explants. These results suggest that ET-1 at low concentration can protect the microsomal CCT activity and reduce the inhibition of PS lipid synthesis induced by oxidant lung injury. The protective mechanism of ET-1 is not relative to the pulmonary endogenous antioxidant defense system.

Effects of vasoactive intestinal peptide on chemotaxis of bronchial epithelial cells / 生理学报

To investigate the influence of vasoactive intestinal peptide (VIP) on chemotaxis of bronchial epithelial cells (BECs). Rabbit chemotactic migration of primary BEC was assessed in a blind-well Boyden chamber. Radioimmunoassay and radio-ligand affinity analysis were used for determining VIP secretion and vasoactive intestinal peptide receptor (VIPR) expression. The results showed: (1) the method for determining chemotaxis of BECs by using insulin as chemotactic factor was stable and reproducible (r=0.9703, P<0.01). (2) VIP (0.001-1 micromol/L) elicited chemotaxis of BECs which was substantial and concentration-dependent. The effects of VIP were inhibited by W-7 and H-7 (P<0.01). (3) Heat stress enhanced the secretion of VIP (P<0.01) and upregulated the expression of VIPR on BECs (P<0.05). These results indicate that VIP in the lungs may play an important role in the repair of damaged epithelium, accelerating restoration of the airway to its normal state. Calmodulin and protein kinase C may be involved in the signal transduction of VIP effects.