Fig 2: CircSLC8A1 is reduced under neuroprotection AqPCR measurements of circSLC8A1 and SLC8A1 mRNA after SH-SY treatment of statins or the PF LRRK2 inhibitor, t-test **P = 0.007 and **P = 0.01 for PF-06447475 and *P = 0.047 and *P = 0.0136 for statins for cirSLC8A1 and SLC8A1 mRNA, respectively, n = 3 biological replicas for each condition. Data presented as mean ± SD.B, CProtein gel and quantification of SLC8A1 and Tubulin as a loading control in statin and PF-treated neuronal cell cultures, t-test *P = 0.027 for statins and *P = 0.011 for PF-06447475, n = 3 biological replicas for each condition. Data presented as mean ± SD.DSLC8A1 immunostaining of statin-treated SH-SY cells.

Fig 3: T3 ameliorated intracellular Ca2+ overload and prevented the intracellular Ca2+ increase in cardiomyocyte during H/R injury. A, The expression of SERCA2a protein expression in neonatal mouse cardiomyocytes; ß-actin was used for normalization. B, Representative bands quantified in the corresponding bar graph. C, The expression of NCX1 protein expression in neonatal mouse cardiomyocytes; ß-actin was used for normalization. D, Representative bands quantified in the corresponding bar graph. (E and F) Cardiomyocytes were stained individually by Fluo-3/AM dye for intracellular Ca2+. The results were determined with flow cytometry and fluorescence intensity of control in each group. The values were expressed as the mean ± SD three independent experiments. n = 6. ···P <.001, ····P <.0001 vs control; ** P <.01 vs H/R; *** P <.001 vs H/R; ## P <.01 vs H/R + T3, ### P <.001 vs H/R + T3

Fig 4: Effects of hypertension on the expression of disease-relevant mRNAs in Dahl salt-sensitive rats.Dahl salt-sensitive rats were kept on low-salt diet (LSD) or high-salt diet (HSD) for 10 weeks to induce hypertension. mRNA levels of (A) SLC8A1 (gene encoding for NCX), (B) ATP2A2 (gene encoding for Serca2a), (C) brain natriuretic peptide (NPPB), (D) ß-adrenergic receptor 1 (ADRB1), (E) interleukin-6 (IL6) and (F) interleukin-6 receptor (IL6R) were quantified by microarray analysis and normalized to the mean expression level of LSD. Data are shown as mean ± SEM (N = 5/6 rats for LSD/HSD). Indicated p-values were calculated using unpaired t-test (except for B, where a Mann–Whitney test was applied).

Fig 5: TYHX ameliorates H/R-induced SANC damage by regulating mitochondrial energy metabolism/mitochondrial membrane permeability transition pore (mPTP) opening and NCX1.1. (a, b) ELISA to detect the activity of mitochondrial respiratory chain supercomplex I/III. (c–g) ELISA to detect the level of mitochondrial energy metabolism. (h) Open rate of mitochondrial membrane permeability transition pore (mPTP). (i) Immunofluorescence of NCX, *p < 0.05.