Hydroxysafflow Yellow A Inhibits Inflammatory Factors Expression in Acute Lung Injury Mice Induced by Lipopolysaccharide_Chinese Journal of Respiratory and Critical Care Medicine

Authors：

SongLijuan ¹ , ZhuYu ² ^# ,  JinMing ²

1. Clinical Institute of Traditional Chinese Medicine, Shanxi University of Traditional Chinese Medicine, Taiyuan, Shanxi, 030619, China;
2. ;

Corresponding?author：

JinMing, Email: jm64456308@163.com

Keywords：

Hydroxysafflor yellow A; Acute lung injury; lipopolysaccharide

DOI：

10.7507/1671-6205.2016132

Video：

Export PDF Favorites Scan Get Citation

Abstract Full text Figures/Tables Video References Cited by

Objective To study the effects of hydroxysafflow yellow A (HSYA) in inhibiting inflammatory signal transduction in lungs of acute lung injury mice induced by lipopolysaccharide (LPS). Methods Eighty-four male Kunming mice were randomly divided into 7 groups, ie. a sham group, a LPS group, a LPS+3 mg/kg dexamethason (DXM) group, a LPS+6 mg/kg HSYA group, a LPS+15 mg/kg HSYA group, a LPS+37.5 mg/kg HSYA group, and a saline+37.5 mg/kg HSYA group (n=12 in each group). The mice were intraperitoneally pretreated with normal saline or DXM or HSYA 0.5 hour prior to intravenous adminstration of LPS. TNF-α, IL-1β and IL-6 levels in mice serum were measured by ELISA and the mRNA and protein levels of TLR4 in mice lungs were assessed by RT-qPCR and Western blot, respectively. Results After being treated with HSYA in doses of 6 mg/kg, 15 mg/kg, and 37.5 mg/kg, the increased expression levels of TLR4 mRNA and protein induced by LPS were significantly inhibited, as well as the increased expression levels of TNF-α, IL-1β and IL-6. The inhibitoty effect enhanced with the doses of HSYA. DXM could inhibit more significantly the increased expression levels of all the indexes. Conclusion HSYA can inhibit inflammatory signal transduction in acute lung injury mice induced by LPS in a dose-dependent manner, but is less effective than DXM.

Citation： SongLijuan, ZhuYu, JinMing. Hydroxysafflow Yellow A Inhibits Inflammatory Factors Expression in Acute Lung Injury Mice Induced by Lipopolysaccharide. Chinese Journal of Respiratory and Critical Care Medicine, 2016, 15(6): 577-582. doi: 10.7507/1671-6205.2016132 Copy

1.	金鳴, 高子淳, 王繼峰.羥基紅花黃色素A抑制PAF誘發的家兔血小板活化的研究.北京中醫藥大學學報, 2004, 5:32-35.
2.	樸永哲, 金鳴, 臧寶霞.紅花黃色素改善大鼠缺氧心肌能量代謝的研究.中草藥, 2003, 34:436-439.
3.	Pepe PE, Potkin RT, Reus DH, et al. Clinical predicators of the adult respiratory distress syndrome. Am J Surg, 1982, 144:124-130.
4.	謝嵐, 毛欣, 李建剛, 等.降鈣素原在慢性阻塞性肺疾病急性加重期抗生素使用中的指導意義.中國呼吸與危重監護雜志, 2013, 12:237-239.
5.	何權瀛. 2015年修訂版慢性阻塞性肺疾病全球防治創議簡介.中國呼吸與危重監護雜志, 2015, 14:125-127.
6.	Sun CY, Pei CQ, Zang BX, et al. The ability of hydroxysafflor yellow A to attenuate lipopolysaccharide-induced pulmonary inflammatory injury in mice. Phytother Res, 2010, 24:1788-95.
7.	Bhatia M, Brady M, Shokuhi S, et al. Inflammatory mediators in acute pancreatitis. J Pathol, 2000, 190:117-125.
8.	Liu DX, Wang Z, Liu SM, et al. Anti-inflammatory effects of fluoxetine in lipopolysaccharide (LPS)-stimulated microglial cells. Neuropharmacology, 2011, 61:592-599.
9.	Xiang M, Fan J. Pattern recognition receptor dependent mechanisms of acute lung injury. Mol Med, 2010, 16:69-82.
10.	Jin R, Liu L, Zhang S, et al. Role of inflammation and its mediators in acute ischemic stroke. J Cardiovasc Transl Res, 2013, 6:834-851.
11.	Hyakkoku K, Hamanaka J, Tsuruma K, et al. Toll-like receptor 4(TLR4), but not TLR3 or TLR9, knock-out mice have neuroprotective effects against focal cerebral ischemia. Neuroscience, 2010, 171:258-267.
12.	Tu XK, Yang WZ, Shi SS, et al. Baicalin inhibits TLR2/4 signaling pathway in rat brain following permanent cerebral ischemia. Inflammation, 2011, 34:463-470.
13.	Lan L, Tao J, Chen A, et al. Electroacupuncture exerts antiinflammatory effects in cerebral ischemiareperfusion injured rats via suppression of the TLR4/NF-κB pathway. Int J Mol Med, 2013, 31:75-80.
14.	Ma Y, He M, Qiang L. Exercise therapy downregulates the overexpression of TLR4, TLR2, MyD88 and NF-κB after cerebral ischemia in rats. Int J Mol Sci, 2013, 14:3718-3733.
15.	Martins JO, Zanoni FL, Martins DO, et al. Insulin regulates cytokines and intercellular adhesion molecule-1 gene expression through nuclear factor-kappa B activation in LPS-induced acute lung injury in rats. Shock, 2009, 31:404-409.
16.	張宇, 鄭為超.紅花黃素抗炎作用機制研究概況.江蘇中醫藥, 2010, 42:77-79.
17.	McAlees JW, Sanders VM. Hematopoietic protein tyrosine phosphatase mediates beta2-adrenergic receptor-induced regulation of p38 mitogen-activated protein kinase in B lymphocytes. Mol Cell Biol, 2009, 29:675-686.
18.	Horikawa H, Kato TA, Mizoguchi Y, et al. Inhibitory effects of SSRIs on IFN-γ induced microglial activation through the regulation of intracellular calcium. Prog Neuropsychopharmacol Biol Psychiatry, 2010, 34:1306-1316.
19.	Song L, Zhu Y, Jin M, et al. Hydroxysafflor yellow A inhibits lipopolysaccharide-induced inflammatory signal transduction in human alveolar epithelial A549 cells. Fitoterapia, 2013, 84:107-114.
20.	朱煜, 宋麗娟, 臧寶霞, 等.羥基紅花黃色素A緩解脂多糖誘導內皮細胞炎癥因子表達升高的研究.心肺血管病雜志, 2012, 30:484-487.

1. 金鳴, 高子淳, 王繼峰.羥基紅花黃色素A抑制PAF誘發的家兔血小板活化的研究.北京中醫藥大學學報, 2004, 5:32-35.
2. 樸永哲, 金鳴, 臧寶霞.紅花黃色素改善大鼠缺氧心肌能量代謝的研究.中草藥, 2003, 34:436-439.
3. Pepe PE, Potkin RT, Reus DH, et al. Clinical predicators of the adult respiratory distress syndrome. Am J Surg, 1982, 144:124-130.
4. 謝嵐, 毛欣, 李建剛, 等.降鈣素原在慢性阻塞性肺疾病急性加重期抗生素使用中的指導意義.中國呼吸與危重監護雜志, 2013, 12:237-239.
5. 何權瀛. 2015年修訂版慢性阻塞性肺疾病全球防治創議簡介.中國呼吸與危重監護雜志, 2015, 14:125-127.
6. Sun CY, Pei CQ, Zang BX, et al. The ability of hydroxysafflor yellow A to attenuate lipopolysaccharide-induced pulmonary inflammatory injury in mice. Phytother Res, 2010, 24:1788-95.
7. Bhatia M, Brady M, Shokuhi S, et al. Inflammatory mediators in acute pancreatitis. J Pathol, 2000, 190:117-125.
8. Liu DX, Wang Z, Liu SM, et al. Anti-inflammatory effects of fluoxetine in lipopolysaccharide (LPS)-stimulated microglial cells. Neuropharmacology, 2011, 61:592-599.
9. Xiang M, Fan J. Pattern recognition receptor dependent mechanisms of acute lung injury. Mol Med, 2010, 16:69-82.
10. Jin R, Liu L, Zhang S, et al. Role of inflammation and its mediators in acute ischemic stroke. J Cardiovasc Transl Res, 2013, 6:834-851.
11. Hyakkoku K, Hamanaka J, Tsuruma K, et al. Toll-like receptor 4(TLR4), but not TLR3 or TLR9, knock-out mice have neuroprotective effects against focal cerebral ischemia. Neuroscience, 2010, 171:258-267.
12. Tu XK, Yang WZ, Shi SS, et al. Baicalin inhibits TLR2/4 signaling pathway in rat brain following permanent cerebral ischemia. Inflammation, 2011, 34:463-470.
13. Lan L, Tao J, Chen A, et al. Electroacupuncture exerts antiinflammatory effects in cerebral ischemiareperfusion injured rats via suppression of the TLR4/NF-κB pathway. Int J Mol Med, 2013, 31:75-80.
14. Ma Y, He M, Qiang L. Exercise therapy downregulates the overexpression of TLR4, TLR2, MyD88 and NF-κB after cerebral ischemia in rats. Int J Mol Sci, 2013, 14:3718-3733.
15. Martins JO, Zanoni FL, Martins DO, et al. Insulin regulates cytokines and intercellular adhesion molecule-1 gene expression through nuclear factor-kappa B activation in LPS-induced acute lung injury in rats. Shock, 2009, 31:404-409.
16. 張宇, 鄭為超.紅花黃素抗炎作用機制研究概況.江蘇中醫藥, 2010, 42:77-79.
17. McAlees JW, Sanders VM. Hematopoietic protein tyrosine phosphatase mediates beta2-adrenergic receptor-induced regulation of p38 mitogen-activated protein kinase in B lymphocytes. Mol Cell Biol, 2009, 29:675-686.
18. Horikawa H, Kato TA, Mizoguchi Y, et al. Inhibitory effects of SSRIs on IFN-γ induced microglial activation through the regulation of intracellular calcium. Prog Neuropsychopharmacol Biol Psychiatry, 2010, 34:1306-1316.
19. Song L, Zhu Y, Jin M, et al. Hydroxysafflor yellow A inhibits lipopolysaccharide-induced inflammatory signal transduction in human alveolar epithelial A549 cells. Fitoterapia, 2013, 84:107-114.
20. 朱煜, 宋麗娟, 臧寶霞, 等.羥基紅花黃色素A緩解脂多糖誘導內皮細胞炎癥因子表達升高的研究.心肺血管病雜志, 2012, 30:484-487.

Chinese Journal of Respiratory and Critical Care Medicine

Hydroxysafflow Yellow A Inhibits Inflammatory Factors Expression in Acute Lung Injury Mice Induced by Lipopolysaccharide

Abstract Full text Figures/Tables Video References Cited by

Previous Article

Next Article

Format

Content