Xin Gou1, Jing Wu2, Mingqing Huang3, Yuting Weng1, Tongxin Yang1, Tao Chen1, Guiqing Li1, Kewei Fang4. 1. Department of Urology, The Second Affiliated Hospital of Kunming Medical University, No. 374, Dianmian Dadao, Kunming, Yunnan, 650101, People's Republic of China. 2. Department of Biochemistry and Molecular Biology, The Primary Medicine School of Kunming Medical University, Kunming, 650101, People's Republic of China. 3. Department of Urology, The 2nd Hospital of Kunming Medical University, Kunming, 650101, People's Republic of China. 4. Department of Urology, The Second Affiliated Hospital of Kunming Medical University, No. 374, Dianmian Dadao, Kunming, Yunnan, 650101, People's Republic of China. 2482099228@qq.com.
Abstract
BACKGROUND: Diabetic bladder disease is common complications of diabetes, its symptoms are diverse, can be due to different stages. In this study we investigate the mechanism of miR-128 targeting CB1 expression to mediate the occurrence of diabetic bladder disease. METHODS: Bioinformatics analysis predicts related regulatory factors of miR-128 in diabetic bladder disease. Models of diabetic bladder lesions were constructed in male SD rats by intraperitoneal injection of streptozotocin at 65 mg/kg body weight. The expression of miR-128 and CB1 mRNA in bladder tissues of each group was detected by RT-qPCR, and CB1, NF-KB, p-JNK and Bcl2 protein expression was detected by Western Blotting. We tested the function of the bladder by urodynamics, detected the pathological characteristics of the bladder tissue by HE staining, and verified the targeting relationship between miR-128 and CB1 through the prediction of the biological website, dual luciferase reporter gene assay and RIP. RESULTS: miR-128 was highly expressed in the bladder tissue of diabetic rats. Inhibition of miR-128 could improve the occurrence of diabetic bladder lesions in rats. miR-128 could target the inhibition of CB1 expression, and high expression of CB1 could antagonize miR-128 against diabetic bladder. In the diabetic bladder, miR-128 can regulate the expression of NF-KB and p-JNK through CB1 and affect the level of apoptosis. miR-128 regulates NF-KB/p-JNK through CB1, thus affecting the occurrence of diabetic bladder disease. CONCLUSION: The high expression of miR-128 can down-regulate the expression of CB1, promote the activation of NF-KB and p-JNK, increase the level of apoptosis and promote the occurrence of diabetic bladder disease.
BACKGROUND: Diabetic bladder disease is common complications of diabetes, its symptoms are diverse, can be due to different stages. In this study we investigate the mechanism of miR-128 targeting CB1 expression to mediate the occurrence of diabetic bladder disease. METHODS: Bioinformatics analysis predicts related regulatory factors of miR-128 in diabetic bladder disease. Models of diabetic bladder lesions were constructed in male SD rats by intraperitoneal injection of streptozotocin at 65 mg/kg body weight. The expression of miR-128 and CB1 mRNA in bladder tissues of each group was detected by RT-qPCR, and CB1, NF-KB, p-JNK and Bcl2 protein expression was detected by Western Blotting. We tested the function of the bladder by urodynamics, detected the pathological characteristics of the bladder tissue by HE staining, and verified the targeting relationship between miR-128 and CB1 through the prediction of the biological website, dual luciferase reporter gene assay and RIP. RESULTS: miR-128 was highly expressed in the bladder tissue of diabetic rats. Inhibition of miR-128 could improve the occurrence of diabetic bladder lesions in rats. miR-128 could target the inhibition of CB1 expression, and high expression of CB1 could antagonize miR-128 against diabetic bladder. In the diabetic bladder, miR-128 can regulate the expression of NF-KB and p-JNK through CB1 and affect the level of apoptosis. miR-128 regulates NF-KB/p-JNK through CB1, thus affecting the occurrence of diabetic bladder disease. CONCLUSION: The high expression of miR-128 can down-regulate the expression of CB1, promote the activation of NF-KB and p-JNK, increase the level of apoptosis and promote the occurrence of diabetic bladder disease.