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. 2017 Feb 20;17(1):117.
doi: 10.1186/s12906-017-1637-z.

Bacopa monnieri extract increases rat coronary flow and protects against myocardial ischemia/reperfusion injury

Sirintorn Srimachai  1   2 , Sylvie Devaux  3 , Celine Demougeot  3 , Sarawut Kumphune  4   5 , Nina D Ullrich  6   7 , Ernst Niggli  6 , Kornkanok Ingkaninan  8 , Natakorn Kamkaew  2   9 , C Norman Scholfield  8 , Sompol Tapechum  1 , Krongkarn Chootip  10
Affiliations

Bacopa monnieri extract increases rat coronary flow and protects against myocardial ischemia/reperfusion injury

Sirintorn Srimachai et al. BMC Complement Altern Med. .

Abstract

Background: This study explored Bacopa monnieri, a medicinal Ayurvedic herb, as a cardioprotectant against ischemia/reperfusion injury using cardiac function and coronary flow as end-points.

Methods: In normal isolated rat hearts, coronary flow, left ventricular developed pressure, heart rate, and functional recovery were measured using the Langendorff preparation. Hearts were perfused with either (i) Krebs-Henseleit (normal) solution, (control), or with 30, 100 μg/ml B. monnieri ethanolic extract (30 min), or (ii) with normal solution or extract for 10 min preceding no-perfusion ischemia (30 min) followed by reperfusion (30 min) with normal solution. Infarct volumes were measured by triphenyltetrazolium staining. L-type Ca2+-currents (ICa, L) were measured by whole-cell patching in HL-1 cells, a mouse atrial cardiomyocyte cell line. Cytotoxicity of B. monnieri was assessed in rat isolated ventricular myocytes by trypan blue exclusion.

Results: In normally perfused hearts, B. monnieri increased coronary flow by 63 ± 13% (30 μg/ml) and 216 ± 21% (100 μg/ml), compared to control (5 ± 3%) (n = 8-10, p < 0.001). B. monnieri treatment preceding ischemia/reperfusion improved left ventricular developed pressure by 84 ± 10% (30 μg/ml), 82 ± 10% (100 μg/ml) and 52 ± 6% (control) compared to pre- ischemia/reperfusion. Similarly, functional recovery showed a sustained increase. Moreover, B. monnieri (100 μg/ml) reduced the percentage of infarct size from 51 ± 2% (control) to 25 ± 2% (n = 6-8, p < 0.0001). B. monnieri (100 μg/ml) reduced ICa, L by 63 ± 4% in HL-1 cells. Ventricular myocyte survival decreased at higher concentrations (50-1000 μg/ml) B. monnieri.

Conclusions: B. monnieri improves myocardial function following ischemia/reperfusion injury through recovery of coronary blood flow, contractile force and decrease in infarct size. Thus this may lead to a novel cardioprotectant strategy.

Keywords: Bacopa monnieri; Brahmi; Cardiac function; Coronary blood flow; Heart; Ischemia/reperfusion; Myocardial infarction.

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Figures

Fig. 1
Fig. 1
B. monnieri improved hemodynamics in isolated rat hearts. a coronary flow (ml/min) using normal perfusate (control) and perfusate containing 30 or 100 μg/ml B. monnieri extract for 30 min, b coronary flow, %, c LVDP, %, d HR, %: b-d expressed as percentage of mean data from the same heart compared to the 10 min stabilization using normal perfusate and e mean expressed as the average of each parameter after application of normal perfusate or perfusate containing B. monnieri extract for 15 min onward. Data are expressed as mean ± SEM (n = 8-10 hearts) and *p < 0.05, **p < 0.001 for 30, 100 μg/ml B. monnieri compared to control, ## p < 0.001 for 30 μg/ml compared to 100 μg/ml B. monnieri
Fig. 2
Fig. 2
Pretreatment with B. monnieri and recovery after myocardial ischemia in isolated rat hearts. a coronary flow (ml/min) using normal perfusate (control) or perfusate containing 30 or 100 μg/ml B. monnieri (10 min), followed by cessation of perfusion (30 min, ischemia) and then restoration of normal perfusate (30 min, reperfusion). b-e truncated time courses showing the post-ischemia recovery period where the values are expressed as percentage of the mean data from the same heart compared to the 10 min stabilization using normal perfusate for b coronary flow, %, c LVDP, %, d HR, % and e functional recovery, %, a global index of cardiac contractile function, calculated as [(HR TRx × LVDP TRx × 100) / HR TP10 × LVDP TP10] where TRx represents the time of reperfusion at x min and TP10 relates to the value at 10 min of the perfusion during stabilization period. Data are expressed as mean ± SEM (n = 9 hearts) and **p < 0.001 for 30 or 100 μg/ml B. monnieri compared to control
Fig. 3
Fig. 3
The sensitivity to myocardial infarction in rat hearts subjected to global ischemia/reperfusion, in the presence or absence of 100 μg/ml B. monnieri. The data shown is the normalised infarction volume of isolated rat hearts in the presence of 100 μg/ml B. monnieri extract for 30 min before the onset of 30-min global ischemia followed by 2 h of reperfusion. The bar graphs represent means ± SEMs (n = 8 for control and n = 6 for B. monnieri extract, **p < 0.0001 vs control)
Fig. 4
Fig. 4
For whole cell currents in voltage clamped HL-1 cardiac cells, K+-currents were blocked by intracellular and extracellular Cs2+, and Na+- and T-currents inactivated by a -40 mV holding potential, then ICa, L activated by stepping to +10 mV (voltage profile: see inset). a Typical trace showing inhibition of ICa, L by 100 μg/ml B. monnieri in the same cell. b Inhibition by 100 μg/ml B. monnier of ICa, L expressed as percentage of mean compared to average of control ICa, L from the same cell. Data are means ± SEM (n = 4 cells from 3 cultures) and *** p < 0.001 comparing B. monnieri vs control, paired t-test
Fig. 5
Fig. 5
Toxicity testing of B. monnieri extract (10–1000 μg/ml) for 1 h on rat freshly isolated ventricular myocyte viability quantified by the trypan blue exclusion assay. Data are expressed as mean ± SEM (n = 3) and *p < 0.05, **p < 0.01 ***p < 0.001 for B. monnieri compared to control
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