[Altered expression of L-type calcium channel alpha1C and alpha1D subunits in colon of rats with diarrhea-predominant irritable bowel syndrome].

OBJECTIVE

To investigate the molecular identities of L-type calcium channel alpha1C subunit (Cav1.2) and alpha1D subunit (Cav1.3) responsible for motor dysfunction of diarrhea-predominant irritable bowel syndrome (D-IBS).

METHODS

A total of 30 male Wistar rats were randomly divided into two groups. The traditional method for irritable bowel syndrome in a cold environment and intragastric administration of Folium Cassiae were combined to develop the D-IBS model. The fecal particles of rats and the water content in feces were measured. Then the expression of Cav1.2 and Cav1.3 mRNA was detected by reverse transcription polymerase chain reaction. The expressions of Cav1.2 and Cav1.3 were examined by immunohistochemistry in colonic tissues from D-IBS model rats and matched tissues.

RESULTS

The fecal particles and the water content in feces of D-IBS model rats significantly increased as compared with the normal rats (6.8 +/- 1.4 vs 3.2 +/- 0.8, P = 0.032, 80% +/- 4% vs 47% +/- 5%, P = 0.018). Cav1.2 and Cav1.3 were positively expressed in colon of both model group and control group rats. The immunohistochemical scores of Cav1.2 and Cav1.3 expression increased in colon of D-IBS model rats as compared with those in normal control rats (3.43 +/- 0.92 vs 2.82 +/- 0.60, P = 0.034, 4.32 +/- 0.51 vs 3.75 +/- 1.05, P = 0.039). The immunohistochemical scores of Cav1.3 expression were significantly higher than Cav1.2 in colon of both two group rats (P = 0.003, 0.005). Similarly, the expression of Cav1.2 and Cav1.3 mRNA increased in colon of D-IBS model rats as compared with those in normal control rats (1.18 +/- 0.15 vs 1.06 +/- 0.12, P = 0.023, 1.32 +/- 0.13 vs 1.23 +/- 0.13, P = 0.033). The expression of Cav1.3 mRNA was significantly higher than Cav1.2 in colon of both two group rats (P = 0.038, 0.012).

CONCLUSIONS

The traditional modeling of irritable bowel syndrome in rats alters the expression of Cav1.2 and Cav1.3. It may be directly related to the generation of enhanced colonic contraction in D-IBS. In addition, Cav1.3 may play a more important role than Cav1.2 in colonic contractility. It offers another potential therapeutic target in the treatment of irritable bowel syndrome.