These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Investigating the mechanism of interactive regulation of B-cell lymphoma-2/Beclin 1 through electroacupuncture intervention during reperfusion in myocardial ischemia-reperfusion injury in a rat model.
    Author: Zhong Z, He P, Hua H, Bai H, Zhang H, Lu S, Qiu W, Gu Y, Qin X.
    Journal: J Physiol Pharmacol; 2022 Dec; 73(6):. PubMed ID: 37087569.
    Abstract:
    To observe the regulation of B-cell lymphoma-2 (Bcl-2)/Beclin 1 interaction through electroacupuncture (EA) intervention during reperfusion and to investigate the EA mechanism of apoptosis-autophagy interactive regulation against myocardial ischemia-reperfusion injury (MIRI). A total of 48 adult Sprague Dawley (SD) rats were randomly divided into the sham-operated group (group Sham), the model group (group Model), the EA group (group EA), and the JNK inhibitor (SP600125) group (group JNK), with 12 rats in each group. Biospecimens were collected randomly from six rats in each group four hours after reperfusion. Evans Blue and triphenyl tetrazolium chloride double-staining were applied to observe each group's myocardial damage area and risk area. We collected 4 ml of blood by abdominal aortic method to detect serum troponin cTnI level by enzyme-linked immunosorbent assay (ELISA). For the remaining six in each group, a part of myocardial tissue below the ligation line was stored in 4% paraformaldehyde for immunohistochemistry and TUNEL staining; the other amount of myocardial tissue was detected by Western blotting to determine the expression levels of Bcl-2, Beclin1, and the phosphorylation levels of Thr69, Ser70, and Ser87 in Bcl-2. In results: electroacupuncture (EA) intervention during reperfusion significantly reduced the myocardial infarction area, cTnI level, and myocardial apoptosis, upregulated Bcl-2 expression, downregulated Beclin 1 expression and inhibited phosphorylation levels of Thr69, Ser70, and Ser87 in Bcl-2. We concluded that EA effectively inhibited apoptosis by upregulating Bcl-2 expression and inhibiting the phosphorylation of Thr69, Ser70, and Ser87 in Bcl-2. This reduced the separation of Bcl-2 and Beclin 1, restrains excessive autophagy, alleviates MIRI, and has a protective effect on myocardial tissue.
    [Abstract] [Full Text] [Related] [New Search]