PMID- 37838934
OWN - NLM
STAT- MEDLINE
DCOM- 20231101
LR  - 20231121
IS  - 1735-8604 (Electronic)
IS  - 1735-8582 (Linking)
VI  - 17
IP  - 5
DP  - 2023 Sep
TI  - The Effect of Moringa Isothiocyanate-1 on Renal Damage in Diabetic Nephropathy.
PG  - 245-254
AB  - INTRODUCTION: Diabetic nephropathy (DN) is the most common clinical complication 
      of diabetes mellitus. Moringa isothiocyanate-1 (MIC-1) is effective in the 
      treatment of diabetes mellitus, but its mechanism of action in DN remains 
      obscure. This research specifically probed the role of MIC-1 in modulating renal 
      injury in DN. METHODS: Six db/m mice were assigned to control group and twelve 
      db/db mice were randomly allocated to the db/db and db/db + MIC-1 groups. The 
      body and kidney weights of the mice were monitored. Renal function indicators and 
      oxidative stress-related markers were assessed by automatic biochemical analyzer 
      and ELISA method. The pathological changes, apoptosis of renal tissues, 
      extracellular regulated protein kinases (ERK) 1/2/ Nuclear factor 
      erythroid2-related factor 2 (Nrf2) pathway-related markers, and the positive 
      expressions of podocalyxin (Pod) and synaptopodin (Syn) were measured by H&E, 
      PAS, and TUNEL staining, Western blot, and IHC assay. RESULTS: MIC-1 reduced the 
      body and kidney weights, and increased the kidney organ index (calculated as 
      100*kidney weight/ body weight) in db/db mice. In addition, MIC-1 improved renal 
      function, kidney tissue injury, and apoptosis of db/db mice. MIC1 noticeably 
      repressed the contents of reactive oxygen species (ROS) and malondialdehyde (MDA) 
      and enhanced the contents of (glutathione) GSH, superoxide dismutase (SOD), and 
      catalase (CAT) in db/db mice. At molecular level, db/db mice showed a decrease in 
      p-ERK/ERK, Nrf2, SOD-1, heme oxygenase 1 (HO-1), and CAT and an increase in p- 
      inhibitor kappa B alpha (IKBalpha) and p-Nuclear factor-kappa B (P65/P65), which were 
      reversed when MIC-1 was administered. Furthermore, MIC-1 facilitated the positive 
      expressions of Pod and Syn of the kidney tissues in db/db mice. CONCLUSION: MIC-1 
      reduces oxidative stress and renal injury by activating the ERK/Nrf2/HO-1 
      signaling and repressing the NFkappaB signaling in db/db mice.  DOI: 
      10.52547/ijkd.7515.
FAU - Chen, Lijing
AU  - Chen L
FAU - Fan, Deyong
AU  - Fan D
FAU - Guo, Fei
AU  - Guo F
FAU - Deng, Jiuhong
AU  - Deng J
FAU - Fu, Linlin
AU  - Fu L
AD  - Department of Pathology, Huzhou Central Hospital and Affiliated Central Hospital 
      Huzhou University, 313000 Huzhou, Zhejiang, China. fulinlin2000@163.com.
LA  - eng
PT  - Comment
PT  - Journal Article
PL  - Iran
TA  - Iran J Kidney Dis
JT  - Iranian journal of kidney diseases
JID - 101316967
RN  - 0 (NF-E2-Related Factor 2)
RN  - GAN16C9B8O (Glutathione)
RN  - 0 (Isothiocyanates)
SB  - IM
CON - AAPS J. 2019 Feb 19;21(2):31. PMID: 30783799
MH  - Mice
MH  - Animals
MH  - *Diabetic Nephropathies/drug therapy/etiology/metabolism
MH  - NF-E2-Related Factor 2/metabolism/pharmacology/therapeutic use
MH  - *Moringa/metabolism
MH  - Kidney
MH  - Oxidative Stress
MH  - Glutathione
MH  - Isothiocyanates/pharmacology/metabolism/therapeutic use
MH  - *Diabetes Mellitus
EDAT- 2023/10/15 12:42
MHDA- 2023/11/01 12:45
CRDT- 2023/10/15 06:34
PHST- 2022/12/13 00:00 [received]
PHST- 2023/07/13 00:00 [accepted]
PHST- 2023/06/08 00:00 [revised]
PHST- 2023/11/01 12:45 [medline]
PHST- 2023/10/15 12:42 [pubmed]
PHST- 2023/10/15 06:34 [entrez]
AID - 7515/1443 [pii]
PST - ppublish
SO  - Iran J Kidney Dis. 2023 Sep;17(5):245-254.