Effects of cyanidin 3-O-glucoside and hydrochlorothiazide on T-cell phenotypes and function in spontaneously hypertensive rats
2020
Aloud, Basma Milad | Petkau, Jay C. | Yu, Liping | McCallum, Jason | Kirby, Chris | Netticadan, Thomas | Blewett, Heather
Immune system dysfunction may contribute to the pathogenesis of hypertension in spontaneously hypertensive rats (SHR). We examined the effects of the anthocyanin, cyanidin 3-O-glucoside (C3G), and the diuretic, hydrochlorothiazide (HCT), on T-cell function in SHR. Five-week-old male SHR and Wistar–Kyoto (WKY) rats received water (n = 8/SHR; n = 8/WKY), 10 mg kg⁻¹ day⁻¹ C3G (n = 8/SHR; n = 8/WKY), 10 mg kg⁻¹ day⁻¹ HCT (n = 8/SHR; n = 8/WKY), or 10 mg kg⁻¹ day⁻¹ C3G + 10 mg kg⁻¹ day⁻¹ HCT (n = 8/SHR; n = 8/WKY) by oral gavage for 15 weeks. Spleens were used to assess T-cell phenotypes via flow cytometry and concanavalin A stimulated ex vivo cytokine production (IL-2, IL-10, TNFα, IFNγ) using a cytometric bead array. SHR had lower proportions of helper T-cells (Th) that were T-regulatory, CD62Lˡᵒ, CD62L⁻ and CD25⁺ compared to WKY. C3G treated SHR had higher proportions of Th that were CD62Lˡᵒ and CD62L⁻, while HCT treated rats had higher CD62Lʰⁱ and CD62Lˡᵒ and lower CD62L⁻ compared to SHR control. The proportion of T-regulatory and Th that were CD25⁺ were not affected by treatment in SHR. Stimulated splenocytes from SHR produced lower concentrations of cytokines compared to WKY. C3G treated SHR produced higher while HCT treated SHR produced lower TNFα and IFNγ concentrations compared to controls. Our findings suggest that C3G has positive effects, whereas HCT further suppresses T-cell function in SHR.
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