1,2,3,4,6‑penta‑O‑galloyl‑β‑D‑glucose alleviates inflammation and oxidative stress in diabetic nephropathy rats through MAPK/NF‑κB and ERK/Nrf2/HO‑1 signaling pathways
Copyright: © Wang et al..
Diabetic nephropathy (DN) is one of the main causes of chronic renal failure, which is also the final cause of mortality in ~30% of diabetic patients. 1, 2, 3, 4, 6-penta-O-galloyl-β-D-glucose (PGG) from Galla rhois has anti-inflammation, anti-oxidation and angiogenesis effects. The present study aimed to explore the protective effects on diabetic nephropathy rats by alleviating inflammation and oxidative stress and the underlying mechanism. High-fat diet/STZ induced rats and high glucose (HG) induced podocytes (MPC5) were used to simulate the DN in vivo and in vitro. The blood glucose level was measured using a blood glucose meter and renal function was determined by an automatic biochemical analyzer. The pathological changes and renal fibrosis were observed through hematoxylin and eosin, periodic acid-Schiff and Masson staining. The expression of nephrin in tissues, fibrosis-related proteins in tissues, MAPK/NF-κB and ERK/nuclear factor erythroid-derived 2-related factor 2 (Nrf2)/hemeoxygenase-1 (HO-1) signaling pathway related proteins in tissues and apoptosis related proteins in tissues and podocytes was detected by western blotting. The inflammatory response and oxidative stress in tissues and podocytes were determined by respective commercial kits and apoptosis in tissues and podocytes was detected by TUNEL assay. The viability of podocytes treated with PGG with or without HG was analyzed by CCK-8 assay. As a result, the blood glucose level, urinary albumin/creatinine ratio, blood urea nitrogen and serum creatinine in blood were all increased and nephrin expression was decreased. The pathological changes and renal fibrosis were aggravated and the inflammation, oxidative stress and apoptosis in renal tissues were enhanced. The above effects were reversed by PGG treatment dose-dependently. MAPK/NF-κB and ERK/Nrf2/HO-1 signaling pathways were activated in DN rats and were suppressed by PGG treatment. The reduced viability and increased apoptosis, inflammation and oxidative stress in MPC5 cells were shown in HG induction, which was reversed by PGG treatment. However, P79350 (p38 agonist) and LM22B-10 (ERK1/2 agonist) weakened the effect of PGG. In conclusion, PGG protects against DN kidney injury by alleviating inflammation and oxidative stress by suppressing the MAPK/NF-κB and ERK/Nrf2/HO-1 signaling pathways.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2022 |
|---|---|
| Erschienen: |
2022 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:24 |
|---|---|
| Enthalten in: |
Experimental and therapeutic medicine - 24(2022), 4 vom: 28. Okt., Seite 639 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Wang, Dong [VerfasserIn] |
|---|
| Links: |
|---|
| Themen: |
1,2,3,4,6-penta-O-galloyl-β-D-glucose |
|---|
| Anmerkungen: |
Date Revised 28.09.2022 published: Electronic-eCollection Citation Status PubMed-not-MEDLINE |
|---|
| doi: |
10.3892/etm.2022.11576 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM346771374 |
|---|
| LEADER | 01000naa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM346771374 | ||
| 003 | DE-627 | ||
| 005 | 20231226032238.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 231226s2022 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.3892/etm.2022.11576 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n1155.xml |
| 035 | |a (DE-627)NLM346771374 | ||
| 035 | |a (NLM)36160883 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Wang, Dong |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a 1,2,3,4,6‑penta‑O‑galloyl‑β‑D‑glucose alleviates inflammation and oxidative stress in diabetic nephropathy rats through MAPK/NF‑κB and ERK/Nrf2/HO‑1 signaling pathways |
| 264 | 1 | |c 2022 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Revised 28.09.2022 | ||
| 500 | |a published: Electronic-eCollection | ||
| 500 | |a Citation Status PubMed-not-MEDLINE | ||
| 520 | |a Copyright: © Wang et al. | ||
| 520 | |a Diabetic nephropathy (DN) is one of the main causes of chronic renal failure, which is also the final cause of mortality in ~30% of diabetic patients. 1, 2, 3, 4, 6-penta-O-galloyl-β-D-glucose (PGG) from Galla rhois has anti-inflammation, anti-oxidation and angiogenesis effects. The present study aimed to explore the protective effects on diabetic nephropathy rats by alleviating inflammation and oxidative stress and the underlying mechanism. High-fat diet/STZ induced rats and high glucose (HG) induced podocytes (MPC5) were used to simulate the DN in vivo and in vitro. The blood glucose level was measured using a blood glucose meter and renal function was determined by an automatic biochemical analyzer. The pathological changes and renal fibrosis were observed through hematoxylin and eosin, periodic acid-Schiff and Masson staining. The expression of nephrin in tissues, fibrosis-related proteins in tissues, MAPK/NF-κB and ERK/nuclear factor erythroid-derived 2-related factor 2 (Nrf2)/hemeoxygenase-1 (HO-1) signaling pathway related proteins in tissues and apoptosis related proteins in tissues and podocytes was detected by western blotting. The inflammatory response and oxidative stress in tissues and podocytes were determined by respective commercial kits and apoptosis in tissues and podocytes was detected by TUNEL assay. The viability of podocytes treated with PGG with or without HG was analyzed by CCK-8 assay. As a result, the blood glucose level, urinary albumin/creatinine ratio, blood urea nitrogen and serum creatinine in blood were all increased and nephrin expression was decreased. The pathological changes and renal fibrosis were aggravated and the inflammation, oxidative stress and apoptosis in renal tissues were enhanced. The above effects were reversed by PGG treatment dose-dependently. MAPK/NF-κB and ERK/Nrf2/HO-1 signaling pathways were activated in DN rats and were suppressed by PGG treatment. The reduced viability and increased apoptosis, inflammation and oxidative stress in MPC5 cells were shown in HG induction, which was reversed by PGG treatment. However, P79350 (p38 agonist) and LM22B-10 (ERK1/2 agonist) weakened the effect of PGG. In conclusion, PGG protects against DN kidney injury by alleviating inflammation and oxidative stress by suppressing the MAPK/NF-κB and ERK/Nrf2/HO-1 signaling pathways | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a 1,2,3,4,6-penta-O-galloyl-β-D-glucose | |
| 650 | 4 | |a diabetic nephropathy | |
| 650 | 4 | |a inflammation | |
| 650 | 4 | |a oxidative stress | |
| 700 | 1 | |a Li, Yan |e verfasserin |4 aut | |
| 700 | 1 | |a Dai, Liheng |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Yanxia |e verfasserin |4 aut | |
| 700 | 1 | |a Zhao, Congna |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Wangang |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Yu |e verfasserin |4 aut | |
| 700 | 1 | |a Zhao, Yinrui |e verfasserin |4 aut | |
| 700 | 1 | |a Yu, Tingting |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Experimental and therapeutic medicine |d 2010 |g 24(2022), 4 vom: 28. Okt., Seite 639 |w (DE-627)NLM206343205 |x 1792-1015 |7 nnns |
| 773 | 1 | 8 | |g volume:24 |g year:2022 |g number:4 |g day:28 |g month:10 |g pages:639 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.3892/etm.2022.11576 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 24 |j 2022 |e 4 |b 28 |c 10 |h 639 | ||