PMID- 32308459
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20240328
IS  - 1178-7007 (Print)
IS  - 1178-7007 (Electronic)
IS  - 1178-7007 (Linking)
VI  - 13
DP  - 2020
TI  - Effects of Hydroxysafflor Yellow A on the PI3K/AKT Pathway and Apoptosis of 
      Pancreatic beta-Cells in Type 2 Diabetes Mellitus Rats.
PG  - 1097-1107
LID - 10.2147/DMSO.S246381 [doi]
AB  - BACKGROUND AND AIM: Type 2 diabetes mellitus (T2DM), a complex metabolic disease, 
      has become a major public health issue around the world. Hydroxysafflor yellow A 
      (HSYA) is the major active chemical ingredient of Carthamus tinctorius 
      L. (safflower), which is widely used in patients with cardiovascular and 
      cerebrovascular diseases in China. The aim of this study was to investigate the 
      anti-diabetic effect and potential mechanism of HSYA on the high-fat diet (HFD) 
      and streptozotocin (STZ-)-induced T2DM rats. MATERIALS AND METHODS: T2DM rats 
      were induced by feeding HFD (60% fat) for four weeks followed by intraperitoneal 
      injection of a low dose of streptozocin (35mg/kg). The T2DM rats were treated 
      with HSYA (120mg/kg) or metformin (90mg/kg) for eight weeks. Biochemical 
      analysis, histological analysis and Western blot analysis were conducted after 8 
      weeks of intervention. RESULTS: The treatment with HSYA evidently reduced 
      fasting-blood glucose and insulin resistance in T2DM rats, indicated by results 
      from fasting-blood glucose, oral glucose tolerance test, fasting insulin levels 
      and histology of pancreas islets. The Western blot results revealed that HSYA 
      reversed the down-regulation of PI3K and AKT in liver. The TUNEL assay analysis 
      of pancreatic tissue showed that HSYA could inhibit the apoptosis of pancreatic 
      beta-cells to a certain extent. Moreover, HSYA-treatment increased the levels of 
      glycogen synthase and hepatic glycogen and improved lipid metabolism by reducing 
      the triglyceride, total and low-density lipoprotein cholesterol levels, even 
      though it did not change the rats' body weights. CONCLUSION: The results of this 
      study suggested that HSYA could promote PI3K/Akt activation and inhibit the 
      apoptosis of pancreatic beta-cells directly or indirectly, which might be the 
      underlying mechanisms in HSYA to improve insulin resistance and regulate 
      glycolipid metabolism in T2DM rats.
CI  - (c) 2020 Lee et al.
FAU - Lee, Maosheng
AU  - Lee M
AUID- ORCID: 0000-0001-7354-447X
AD  - The Fourth Clinical Medical College, Guangzhou University of Chinese Medicine, 
      Guangzhou 510006, People's Republic of China.
AD  - Department of Endocrinology, Shenzhen Traditional Chinese Medicine Hospital, 
      Shenzhen 518033, People's Republic of China.
FAU - Li, Huilin
AU  - Li H
AD  - Department of Endocrinology, Shenzhen Traditional Chinese Medicine Hospital, 
      Shenzhen 518033, People's Republic of China.
FAU - Zhao, Hengxia
AU  - Zhao H
AD  - Department of Endocrinology, Shenzhen Traditional Chinese Medicine Hospital, 
      Shenzhen 518033, People's Republic of China.
FAU - Suo, Miao
AU  - Suo M
AUID- ORCID: 0000-0001-7435-4571
AD  - The Fourth Clinical Medical College, Guangzhou University of Chinese Medicine, 
      Guangzhou 510006, People's Republic of China.
AD  - Department of Endocrinology, Shenzhen Traditional Chinese Medicine Hospital, 
      Shenzhen 518033, People's Republic of China.
FAU - Liu, Deliang
AU  - Liu D
AUID- ORCID: 0000-0003-3777-6489
AD  - Department of Endocrinology, Shenzhen Traditional Chinese Medicine Hospital, 
      Shenzhen 518033, People's Republic of China.
LA  - eng
PT  - Journal Article
DEP - 20200409
PL  - New Zealand
TA  - Diabetes Metab Syndr Obes
JT  - Diabetes, metabolic syndrome and obesity : targets and therapy
JID - 101515585
PMC - PMC7154009
OTO - NOTNLM
OT  - PI3K/AKT pathway
OT  - apoptosis
OT  - hydroxysafflor yellow A
OT  - insulin resistance
OT  - traditional Chinese medicine
OT  - type 2 diabetes mellitus
COIS- The authors report no conflicts of interest in this work.
EDAT- 2020/04/21 06:00
MHDA- 2020/04/21 06:01
PMCR- 2020/04/09
CRDT- 2020/04/21 06:00
PHST- 2020/01/17 00:00 [received]
PHST- 2020/03/22 00:00 [accepted]
PHST- 2020/04/21 06:00 [entrez]
PHST- 2020/04/21 06:00 [pubmed]
PHST- 2020/04/21 06:01 [medline]
PHST- 2020/04/09 00:00 [pmc-release]
AID - 246381 [pii]
AID - 10.2147/DMSO.S246381 [doi]
PST - epublish
SO  - Diabetes Metab Syndr Obes. 2020 Apr 9;13:1097-1107. doi: 10.2147/DMSO.S246381. 
      eCollection 2020.