OBJECTIVE: To investigate the signal transduction mechanism of curcumin in inhibiting the proliferation of bovine lens epithelial cell (LEC) induced by recombinant human epidermal growth factor (rhEGF). METHODS: There were three groups in this experiment, which were normal control group, untreated group and curcumin-treated group. Proliferation of LEC was induced by rhEGF (50 microg/L). The concentration of intracellular Ca(2+) ([Ca(2+)](i)) in LEC was measured with Fura-2/AM by spectrofluorimetry. The contents of intracellular cAMP and cGMP were assayed by radioimmunoassay. RESULTS: The [Ca(2+)]i in LEC was obviously increased in the untrated group as compared with that in the normal control group (P<0.01), and the [Ca(2+)](i) in LEC in the curcumin-treated group was highest among three groups (P<0.01). The content of intracellular cAMP in LEC was decreased while the content of intracellular cGMP was obviously increased in the untreated group as compared with those in the normal control group (P<0.01). The content of intracellular cAMP in LEC was higher in the curcumin-treated group than that in the untreated group, while the content of intracellular cGMP was lower than that in the untreated group (P<0.01). CONCLUSION: The antiproliferation effects of curcumin on LEC may relate to the regulations of multiple processes of signal transduction.
OBJECTIVE: To investigate the signal transduction mechanism of curcumin in inhibiting the proliferation of bovine lens epithelial cell (LEC) induced by recombinant humanepidermal growth factor (rhEGF). METHODS: There were three groups in this experiment, which were normal control group, untreated group and curcumin-treated group. Proliferation of LEC was induced by rhEGF (50 microg/L). The concentration of intracellular Ca(2+) ([Ca(2+)](i)) in LEC was measured with Fura-2/AM by spectrofluorimetry. The contents of intracellular cAMP and cGMP were assayed by radioimmunoassay. RESULTS: The [Ca(2+)]i in LEC was obviously increased in the untrated group as compared with that in the normal control group (P<0.01), and the [Ca(2+)](i) in LEC in the curcumin-treated group was highest among three groups (P<0.01). The content of intracellular cAMP in LEC was decreased while the content of intracellular cGMP was obviously increased in the untreated group as compared with those in the normal control group (P<0.01). The content of intracellular cAMP in LEC was higher in the curcumin-treated group than that in the untreated group, while the content of intracellular cGMP was lower than that in the untreated group (P<0.01). CONCLUSION: The antiproliferation effects of curcumin on LEC may relate to the regulations of multiple processes of signal transduction.