Id |
Subject |
Object |
Predicate |
Lexical cue |
T1 |
0-105 |
Sentence |
denotes |
Astragaloside IV attenuates orbital inflammation in Graves' orbitopathy through suppression of autophagy. |
T1 |
0-105 |
Sentence |
denotes |
Astragaloside IV attenuates orbital inflammation in Graves' orbitopathy through suppression of autophagy. |
T2 |
106-119 |
Sentence |
denotes |
INTRODUCTION: |
T2 |
106-119 |
Sentence |
denotes |
INTRODUCTION: |
T3 |
120-219 |
Sentence |
denotes |
Graves' orbitopathy (GO) is an autoimmune inflammatory disorder affecting the orbit around the eye. |
T3 |
120-219 |
Sentence |
denotes |
Graves' orbitopathy (GO) is an autoimmune inflammatory disorder affecting the orbit around the eye. |
T4 |
220-342 |
Sentence |
denotes |
Astragaloside IV (AS-VI) is the main active ingredient of the Chinese herbal medicine Huangqi (Radix Astragali Mongolici). |
T4 |
220-342 |
Sentence |
denotes |
Astragaloside IV (AS-VI) is the main active ingredient of the Chinese herbal medicine Huangqi (Radix Astragali Mongolici). |
T5 |
343-549 |
Sentence |
denotes |
AS-IV exhibits antioxidant and anti-inflammatory properties, and shows therapeutic potential in a number of ischemic and inflammatory diseases; however, its pharmaceutical activities in GO remain undefined. |
T5 |
343-549 |
Sentence |
denotes |
AS-IV exhibits antioxidant and anti-inflammatory properties, and shows therapeutic potential in a number of ischemic and inflammatory diseases; however, its pharmaceutical activities in GO remain undefined. |
T6 |
550-572 |
Sentence |
denotes |
MATERIALS AND METHODS: |
T6 |
550-572 |
Sentence |
denotes |
MATERIALS AND METHODS: |
T7 |
573-838 |
Sentence |
denotes |
In this study, we investigated the effects of AS-IV on interleukin (IL)-1β-induced orbital fibroblast inflammation in vitro and GO orbital inflammation and ocular histopathological changes in vivo, as well as the underlying mechanisms responsible for these effects. |
T7 |
573-838 |
Sentence |
denotes |
In this study, we investigated the effects of AS-IV on interleukin (IL)-1β-induced orbital fibroblast inflammation in vitro and GO orbital inflammation and ocular histopathological changes in vivo, as well as the underlying mechanisms responsible for these effects. |
T8 |
839-862 |
Sentence |
denotes |
RESULTS AND CONCLUSION: |
T8 |
839-862 |
Sentence |
denotes |
RESULTS AND CONCLUSION: |
T9 |
863-1008 |
Sentence |
denotes |
The results show that IL-1β increased mRNA expression of the inflammatory cytokines IL-6, IL-8, TNF-α, and MCP-1 in cultured orbital fibroblasts. |
T9 |
863-1008 |
Sentence |
denotes |
The results show that IL-1β increased mRNA expression of the inflammatory cytokines IL-6, IL-8, TNF-α, and MCP-1 in cultured orbital fibroblasts. |
T10 |
1009-1185 |
Sentence |
denotes |
This IL-1β-induced inflammation was accompanied by increased autophagic activity as reflected in increased Beclin-1 and Agt-5 expression, as well as LC3-I to LC3-II conversion. |
T10 |
1009-1185 |
Sentence |
denotes |
This IL-1β-induced inflammation was accompanied by increased autophagic activity as reflected in increased Beclin-1 and Agt-5 expression, as well as LC3-I to LC3-II conversion. |
T11 |
1186-1457 |
Sentence |
denotes |
Pretreatment with the autophagy inhibitors 3-MA and bafilomycin A1, or silencing of autophagy-related proteins Beclin-1 and Atg-5, prevented IL-1β-induced orbital fibroblast inflammation, while pretreatment with the autophagy activator rapamycin had the opposite effects. |
T11 |
1186-1457 |
Sentence |
denotes |
Pretreatment with the autophagy inhibitors 3-MA and bafilomycin A1, or silencing of autophagy-related proteins Beclin-1 and Atg-5, prevented IL-1β-induced orbital fibroblast inflammation, while pretreatment with the autophagy activator rapamycin had the opposite effects. |
T12 |
1458-1534 |
Sentence |
denotes |
These data suggested that autophagy was involved in GO orbital inflammation. |
T12 |
1458-1534 |
Sentence |
denotes |
These data suggested that autophagy was involved in GO orbital inflammation. |
T13 |
1535-1769 |
Sentence |
denotes |
AS-IV treatment significantly decreased IL-1β-induced inflammatory cytokine production in orbital fibroblasts in vitro and attenuated GO orbital inflammation, fat accumulation, collagen deposition, and macrophage infiltration in vivo. |
T13 |
1535-1769 |
Sentence |
denotes |
AS-IV treatment significantly decreased IL-1β-induced inflammatory cytokine production in orbital fibroblasts in vitro and attenuated GO orbital inflammation, fat accumulation, collagen deposition, and macrophage infiltration in vivo. |
T14 |
1770-1948 |
Sentence |
denotes |
These in vitro and in vivo protective effects of AS-IV against GO were accompanied by decreased autophagic activities in orbital fibroblasts and GO orbital tissues, respectively. |
T14 |
1770-1948 |
Sentence |
denotes |
These in vitro and in vivo protective effects of AS-IV against GO were accompanied by decreased autophagic activities in orbital fibroblasts and GO orbital tissues, respectively. |
T15 |
1949-2050 |
Sentence |
denotes |
Collectively, our findings suggested that AS-IV protects against GO through suppression of autophagy. |
T15 |
1949-2050 |
Sentence |
denotes |
Collectively, our findings suggested that AS-IV protects against GO through suppression of autophagy. |
T16 |
2051-2099 |
Sentence |
denotes |
Thus, AS-IV may have preventive benefits for GO. |
T16 |
2051-2099 |
Sentence |
denotes |
Thus, AS-IV may have preventive benefits for GO. |