Abstract
This study aimed to investigate cerebral cortex apoptosis on the early aged hypertension and the effects of green tea flavonoid epigallocatechin-3-gallate (EGCG). Twenty-four rats were divided into three groups: a control Wistar-Kyoto group (WKY, n = 8), a spontaneously early aged hypertensive group (SHR, n = 8), and an early aged hypertension with EGCG treatment group (SHR-EGCG, n = 8; daily oral EGCG 200 mg/kg—94%, 12 weeks). At 48 weeks old, blood pressures (BPs) were evaluated and cerebral cortexes were isolated for TUNEL assay and Western blotting. Systolic, diastolic, and mean blood pressure levels in the SHR-EGCG were reduced compared to the SHR. The percentage of neural cell deaths, the levels of cytosolic Endonuclease G, cytosolic AIF (Caspase-independent apoptotic pathway), Fas, Fas Ligand, FADD, Caspase-8 (Fas-mediated apoptotic pathway), t-Bid, Bax/Bcl-2, Bak/Bcl-xL, cytosolic Cytochrome C, Apaf-1, Caspase-9 (Mitochondrial-mediated apoptotic pathway), and Caspase-3 (Fas-mediated and Mitochondria-mediated apoptotic pathways) were increased in the SHR relative to WKY and reduced in SHR-EGCG relative to SHR. In contrast, the levels of Bcl-2, Bcl-xL, p-Bad, 14-3-3, Bcl-2/Bax, Bcl-xL/Bak, and p-Bad/Bad (Bcl-2 family-related pro-survival pathway), as well as Sirt1, p-PI3K/PI3K and p-AKT/AKT (Sirt1/PI3K/AKT-related pro-survival pathway), were reduced in SHR relative WKY and enhanced in SHR-EGCG relative to SHR. In conclusion, green tea flavonoid epigallocatechin-3-gallate (EGCG) might prevent neural apoptotic pathways and activate neural survival pathways, providing therapeutic effects on early aged hypertension-induced neural apoptosis.
Highlights
Hypertension is considered as the common cause of mortality (ESC/ESH, 2018)
After 8 weeks of EGCG treatment, the levels of systolic BP (SBP) and mean BP (MBP) in the spontaneously early aged hypertensive group (SHR)-EGCG group were significantly reduced when compared to the SHR group (Figure 1)
After 12 weeks of EGCG treatment, the levels of SBP, diastolic BP (DBP), and MBP in the SHREGCG group were significantly reduced when compared to the SHR group (Table 1 and Figure 1)
Summary
Hypertension is considered as the common cause of mortality (ESC/ESH, 2018). In hypertension, the brain suffers oxidative stress and inflammatory processes, which lead to neurodegeneration characterized by the progressive loss of neurons (Gasecki et al, 2013; Hou et al, 2018). Neural apoptosis is promoted by several major apoptotic pathways, including Endonuclease G (EndoG) and Apoptosis-inducing factor (AIF)-related Caspase-independent apoptotic pathway, Fas-mediated Caspase-dependent apoptotic pathway, and mitochondrial-mediated Caspase-dependent apoptotic pathway (Yakovlev and Faden, 2004). EndoG is the mitochondrial specific endonuclease and the Caspase-independent factor, released into the cytosol in brain damage (Yakovlev and Faden, 2004). The cytosolic EndoG and AIF translocate into the nucleus, activating the neural Caspase-independent apoptotic manner through largescale DNA loss and chromatin condensation (Bastianetto et al, 2011). To the best of our knowledge, the alterations of EndoG and AIF-related Caspase-independent apoptotic pathway in the early aged (48-week-old) hypertensive brain have not been investigated yet
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