Key result
Losartan reduces inflammatory and apoptotic markers in spontaneously hypertensive rats.
Why the study?
Apoptosis is increased in the hypertrophied left ventricle of spontaneously hypertensive rats, potentially due to exaggerated local angiotensin production, but the effects of losartan on related gene expressions are unclear.
Does losartan reduce the expression of inflammatory and apoptotic markers in the left ventricle of spontaneously hypertensive rats?
Does losartan reduce the expression of inflammatory and apoptotic markers in the left ventricle of spontaneously hypertensive rats?
Losartan reduces the expression of inflammatory and apoptotic markers in the hypertrophied left ventricle of spontaneously hypertensive rats.
Losartan may mitigate LV inflammation and apoptosis in hypertensive rat models; leaves open translation to human disease.
PURPOSE: Increased apoptosis was recently found in the hypertrophied left ventricle of spontaneously hypertensive rats (SHRs). Although the available evidence suggests that apoptosis can be induced in cardiac cells by various insults including pressure overload, cardiac apoptosis appears to result from an exaggerated local production of angiotensin in adult SHRs. Altered expressions of Bcl associated X (Bax), Bcl-2, chemokine receptor (CCR)-2, monocyte chemoattractant protein (MCP)-1, transforming growth factor (TGF)-β1, phosphorylated extracellular signal-regulated kinases (PERK), and connexin 43 proteins, and kallikrein mRNA were investigated to explore the effects of losartan on the SHR model. METHODS: Twelve-week-old male rats were grouped as follows: control (C), SHR (hypertension: H), and losartan (L; SHRs were treated with losartan [10 mg/kg/day] for 5 weeks). Western blot and reverse transcription polymerase chain reaction assays were performed. RESULTS: Expression of Bax, CCR-2, MCP-1, TGF-β1, PERK, and connexin 43 proteins, and kallikrein mRNA was significantly increased in the H group compared to that in the C group at weeks 3 and 5. Expression of Bax, CCR-2, MCP-1, TGF-β1, and connexin 43 proteins and kallikrein mRNA was significantly decreased after losartan treatment at week 5. PERK protein expression was significantly decreased after losartan treatment at weeks 3 and 5. Bcl-2 protein expression was significantly decreased in the H group compared to that in the C group at weeks 3 and 5. CONCLUSION: Losartan treatment reduced expression of Bax, CCR-2, MCP-1, TGF-β1, PERK, and connexin 43 proteins, and kallikrein mRNA in SHRs, along with decreased inflammation and apoptosis.
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Lee et al. (2018) studied Hypertension (n=42). Losartan vs. Untreated spontaneously hypertensive rats was evaluated on Bax protein expression level at week 5 (p=<0.05). Losartan treatment significantly reduced the expression of Bax, CCR-2, MCP-1, TGF-β1, PERK, and connexin 43 proteins, and kallikrein mRNA in spontaneously hypertensive rats, indicating decreased inflammation and apoptosis.
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