[Spinal lncRNA_RT1-CE10 attenuates chronic visceral hypersensitivity in rats with irritable bowel syndrome via inhibiting microglial activation].

Abstract

The purpose of the study was to investigate the role of the long non-coding RNA (lncRNA)_RT1-CE10 and its molecular mechanisms in chronic visceral pain of rats with irritable bowel syndrome (IBS). Sprague-Dawley (SD) rats were exposed to colorectal distention (CRD) stimulation at a pressure of 60 mmHg for 1 min from 8 to 14 days after birth. The visceral hypersensitivity was assessed by measuring electromyographic (EMG) responses of external oblique muscle to CRD at 40 mmHg and 60 mmHg when the rats were 6 weeks old. The expression of lncRNA_RT1-CE10, Iba-1 and MHCII in the spinal cord was detected by RT-qPCR or Western blot. After intrathecal injection of minocycline (an inhibitor of microglia), the expression of Iba-1, MHCII and the visceral hypersensitivity were determined by Western blot and EMG, respectively. After intrathecal injection of AAV-lncRT1-CE10 and AAV-shlncRT1-CE10, the expression of Iba-1 and MHCII was examined by Western blot, respectively. The results showed that the expression of lncRNA_RT1-CE10 was decreased in the spinal cord of IBS rats, while the expression of Iba-1 and MHCII was increased. Inhibition of microglial activation by minocycline attenuated visceral hypersensitivity in IBS rats. Over-expression of lncRNA_RT1-CE10 decreased the Iba-1 and MHCⅡ levels in IBS rats, while knockdown of lncRNA_RT1-CE10 increased the Iba-1 and MHCⅡ levels in control rats. Collectively, these results demonstrate that lncRNA_RT1-CE10 attenuates visceral hypersensitivity by inhibiting microglial activation in IBS rats.