Shuang Zhang1, Hong Li, Shi-jie Yang. 1. Department of Pharmacology, Norman Bethune College of Medicine, Jilin University, Changchun, China.
Abstract
AIM: To investigate the protective effect of tribulosin, a monomer of the gross saponins from Tribulus terrestris, against cardiac ischemia/reperfusion injury and the underlying mechanism in rats. METHODS: Isolated rat hearts were subjected to 30 min of ischemia followed by 120 min of reperfusion using Langendorff's technique. The hearts were assigned to seven groups: control, ischemia/reperfusion (I/R), treatment with gross saponins from Tribulus terrestris (GSTT) 100 mg/L, treatment with tribulosin (100, 10, and 1 nmol/L) and treatment with a PKC inhibitor (chelerythrine) (1 micromol/L). Infarct size was assessed by triphenyltetrazolium chloride staining. Malondialdehyde (MDA), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) contents as well as superoxide dismutase (SOD) and creatine kinase (CK) activities were determined after the treatment. Histopathological changes in the myocardium were observed using hematoxylin-eosin (H&E) staining. Apoptosis was detected with terminal deoxynucleotidyl transferase nick-end labeling (TUNEL) assay. Bcl-2, Bax, caspase-3, and PKCepsilon protein expression were examined using Western blotting. RESULTS: Tribulosin treatment significantly reduced MDA, AST, CK and LDH contents, and increased the activity of SOD. The infarct size of I/R group was 40.21% of the total area. GSTT and various concentrations of tribulosin treatment decreased the infarct size to 24.33%, 20.24%, 23.19%, and 30.32% (P<0.01). Tribulosin treatment reduced the myocardial apoptosis rate in a concentration-dependent manner. Bcl-2 and PKCepsilon protein expression was increased after tribulosin preconditioning, whereas Bax and caspase-3 expression was decreased. In the chelerythrine group, Bcl-2 and PKCepsilon expression was decreased, whereas Bax and caspase-3 expression was increased. CONCLUSION: Tribulosin protects myocardium against ischemia/reperfusion injury through PKCepsilon activation.
AIM: To investigate the protective effect of tribulosin, a monomer of the gross saponins from Tribulus terrestris, against cardiac ischemia/reperfusion injury and the underlying mechanism in rats. METHODS: Isolated rat hearts were subjected to 30 min of ischemia followed by 120 min of reperfusion using Langendorff's technique. The hearts were assigned to seven groups: control, ischemia/reperfusion (I/R), treatment with gross saponins from Tribulus terrestris (GSTT) 100 mg/L, treatment with tribulosin (100, 10, and 1 nmol/L) and treatment with a PKC inhibitor (chelerythrine) (1 micromol/L). Infarct size was assessed by triphenyltetrazolium chloride staining. Malondialdehyde (MDA), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) contents as well as superoxide dismutase (SOD) and creatine kinase (CK) activities were determined after the treatment. Histopathological changes in the myocardium were observed using hematoxylin-eosin (H&E) staining. Apoptosis was detected with terminal deoxynucleotidyl transferase nick-end labeling (TUNEL) assay. Bcl-2, Bax, caspase-3, and PKCepsilon protein expression were examined using Western blotting. RESULTS:Tribulosin treatment significantly reduced MDA, AST, CK and LDH contents, and increased the activity of SOD. The infarct size of I/R group was 40.21% of the total area. GSTT and various concentrations of tribulosin treatment decreased the infarct size to 24.33%, 20.24%, 23.19%, and 30.32% (P<0.01). Tribulosin treatment reduced the myocardial apoptosis rate in a concentration-dependent manner. Bcl-2 and PKCepsilon protein expression was increased after tribulosin preconditioning, whereas Bax and caspase-3 expression was decreased. In the chelerythrine group, Bcl-2 and PKCepsilon expression was decreased, whereas Bax and caspase-3 expression was increased. CONCLUSION:Tribulosin protects myocardium against ischemia/reperfusion injury through PKCepsilon activation.
Authors: Y Qiu; P Ping; X L Tang; S Manchikalapudi; A Rizvi; J Zhang; H Takano; W J Wu; S Teschner; R Bolli Journal: J Clin Invest Date: 1998-05-15 Impact factor: 14.808
Authors: K M Lawrence; A M N Kabir; M Bellahcene; S Davidson; X B Cao; J McCormick; R A Mesquita; C J Carroll; A Chanalaris; P A Townsend; M Hubank; A Stephanou; R A Knight; M S Marber; D S Latchman Journal: FASEB J Date: 2005-03-10 Impact factor: 5.191
Authors: P Ping; J Zhang; X Cao; R C Li; D Kong; X L Tang; Y Qiu; S Manchikalapudi; J A Auchampach; R G Black; R Bolli Journal: Am J Physiol Date: 1999-05
Authors: R C Li; P Ping; J Zhang; W B Wead; X Cao; J Gao; Y Zheng; S Huang; J Han; R Bolli Journal: Am J Physiol Heart Circ Physiol Date: 2000-10 Impact factor: 4.733
Authors: Peipei Ping; Changxu Song; Jun Zhang; Yiru Guo; Xinan Cao; Richard C X Li; Wenjian Wu; Thomas M Vondriska; Jason M Pass; Xian-Liang Tang; William M Pierce; Roberto Bolli Journal: J Clin Invest Date: 2002-02 Impact factor: 14.808
Authors: B S Nishchal; S Rai; M N Prabhu; Sheetal D Ullal; S Rajeswari; H N Gopalakrishna Journal: Indian J Pharm Sci Date: 2014 Nov-Dec Impact factor: 0.975
Authors: Traci L Parry; Joseph W Starnes; Sara K O'Neal; James R Bain; Michael J Muehlbauer; Aubree Honcoop; Amro Ilaiwy; Peter Christopher; Cam Patterson; Monte S Willis Journal: Metabolomics Date: 2017-12-04 Impact factor: 4.290