[Effects and mechanisms of total flavones of Abelmoschus manihot in attenuating diabetic tubulopathy by targeting endoplasmic reticulum stress-induced cell apoptosis].

• DOI: 10.19540/j.cnki.cjcmm.20230216.702
• Publication Date: 2023-05-01
• Authors: Bing‐Ying Wan; Dongwei Cao; Yi‐Gang Wan; Chen Dai; Wei Wu; Qi‐Jun Fang; Si-Yi Liu; Yue Tu; Yu Wang; Zi-Yue Wan

Renal tubular injury in patients with diabetic kidney disease(DKD) may be accompanied by glomerular and microvascular diseases. It plays a critical role the progression of renal damage DKD, is now known as tubulopathy(DT). To explore multi-targeted therapeutic effects pharmacological mechanisms vivo total flavones Abelmoschus manihot(TFA), an extract from traditional Chinese medicine for treating disease, attenuating DT, authors randomly divided all rats into four groups: normal control group(normal group), DT model group(model model+TFA-treated group(TFA group) model+rosiglitazone(ROS)-treated group(ROS group). The rat was established based on DKD means integrated measures. After successful modeling, groups were continuously given double-distilled water, TFA suspension, ROS respectively gavage every day. 6 weeks treatment, sacrificed, samples their urine, blood, kidneys collected. various indicators related to urine blood biochemistry, injury, epithelial cell apoptosis endoplasmic reticulum stress(ERS), well activation protein kinase R-like kinase(PERK)-eukaryotic translation initiation factor 2α(eIF2α)-activating transcription 4(ATF4)-C/EBP homologous protein(CHOP) signaling pathway investigated. results indicated that hypertrophy cells, hyperplasia occlusion, interstitial extracellular matrix collagen deposition occurred rats. Moreover, significant changes found expression degree level markers. In addition, there abnormal increase proteins. or protein, characteristics ERS, PERK-eIF2α-ATF4-CHOP improved varying degrees. Therein, superior affecting pathological tubule/interstitium. short, rats, this study demonstrated could attenuate multiple targets through inhibiting ERS-induced vivo, its effect mechanism suppressing kidney. These findings provided preliminary evidence application clinical treatment DT.