Skip to main content
. 2019 Jul 22;2019:8512405. doi: 10.1155/2019/8512405

Table 2.

Basic information on the included studies.

Research Experimental model Observation indicators Effect of XMLI
Wu et al. 1995[10] rabbits with myocardial injury induced by isoproterenol J-point displacement (increased or lowered) on the ECG; frequency of ischemic arrhythmia After pretreatment with XMLI, the J-point displacement on the ECG caused by isoproterenol can be significantly reduced, so that the J-point position is close to the normal equipotential line. And the frequency of ischemic arrhythmia can be significantly reduced.
Wu et al. 2002[11] rats with myocardial injury induced by isoproterenol J-point displacement (increased or decreased) on the ECG; CPK, LDH in serum; MDA, SOD, GSH-PX in myocardial tissue After pretreatment with XMLI, the J-point displacement on the ECG caused by isoproterenol can be significantly reduced, MDA level be reduced, CPK and LDH activity be reduced, GSH-PX and SOD activity be increased.
Tian and Yang 2010[12] rabbits with ischemia-reperfusion induced by hypovolemic shock SOD; NO−2/NO−3; blood pH; urine output XMLI can increase SOD activity and NO2−/NO3− level, correct acidosis, increase blood pH, improve circulating blood flow, and increase urine output.
Li et al. 2017[13] isolated rat heart;
H9C2 cells (rat cardiomyocytes)		 cardiac function; [Ca2+]i of H9C2 under electrical stimulation; Ca2+ influx; intracellular Ca2+ store; T-type Ca2+ channels; NCX; Na+/K+-ATPase activity; ROS; SOD-1; SOD-2; HO-1 XMLI can increase intracellular Ca2+ level by activating T-type Ca2+ channels and inhibiting Na+/K+-ATPase. XMLI can also reduce the production of ROS and enhance the expressions of SOD-1, SOD-2, HO-1.
Cao et al. 2009[14] young rabbits with myocardial ischemia-reperfusion injury CPK; iNOS; ecNOS; MDA XMLI can reduce the ecNOS, MDA, CK activity and inflammatory cell infiltration in the reperfusion injury model.
Zhang et al. 2011[15] asphyxiating newborn rats CK-MB; NF-κB; TNF-α After 6 hours of asphyxia in neonatal rats, serum CK-MB level, myocardial NF-κB, and TNF-α expressions peaked. XMLI can significantly reduce serum CK-MB level, myocardial NF-κB, and TNF-α expressions.
Liu et al. 2014[16] healthy rats for preparing doxorubicin-induced HF model LVEF; LVFS; SOD; MDA; BNP; cTnI XMLI can reduce doxorubicin-induced cardiotoxicity, increase SOD activity and cardiac EF, and decrease MDA activity.
Liu et al. 2016[17] healthy rats for preparing doxorubicin-induced HF model LVEF; LVFS; SOD; MDA; BNP XMLI can reduce doxorubicin-induced cardiotoxicity, increase SOD activity and cardiac EF, and decrease MDA activity.
Duan et al. 2018[18] healthy rats for preparing epirubicin-induced HF model body weight; LVEF; SOD; MDA; BNP; cTnI XMLI can reduce epirubicin-induced cardiotoxicity, increase SOD activity and EF, decrease MDA activity and cTnI level, and prevent weight loss.
Yuan and Jiang 2017[19] H9C2 cells (rat cardiomyocytes) cardiomyocyte activity; SOD; MDA; Caspase-3 activity; autophagy-associated protein LC3B activity XMLI can reduce doxorubicin-induced cardiotoxicity, increase cell activity and SOD activity, and decrease MDA level, Caspase-3 activity, and protein LC3B accumulation.
Li et al. 2016[20] healthy rats for preparing epirubicin-induced HF model cardiac function; survival rate; body weight; LVPW thickness; EF; ECG; accumulation of collagen; expression of MMPs and TIMP4; expression of TGF-β1 mRNAs; expression of Ace, Ace2, Mas, and Agtr1 mRNAs; autophagy; expression of PI3K and AKT; the phosphorylation of P38 MAPK and ERK1/2 XMLI can enhance the survival rate of rats from epirubicin-induced HF. XMLI can prevent LV dilatation, improve cardiac function. And the treatment of the epirubicin rats with XMLI significantly recovered these changes, such as QT, QTc intervals and QRS duration. Furthermore, XMLI can significantly inhibit the accumulation of collagen, reduce the MMP9 and TGF-β1. XMLI can also decrease Beclin1 and Atg7, activate the PI3K/AKT signaling pathway and inhibit the ERK1/2 and P38 MAPK signaling pathways.
Li et al. 2019[21] H9C2 cells (rat cardiomyocytes) IL-1b; IL-6; TNF-α; expression of LC3, PINK1, Parkin, Nix, Beclin-1; Mitofusin1, Mitofusin2, Opa1, Drp1 and P62 XMLI can increase cell viability and the release of LC3 in H9C2 cells. XMLI can reduce the level of cTnI, CK-MB, IL-1b, IL-6, and TNF-α. XMLI can increase the protein and mRNA expression of PINK1, Parkin, Nix, Beclin-1 and decrease expression of Mitofusin1, Mitofusin2, Opa1, Drp1, and P62.
Peng et al. 2002[22] cardiomyocytes of healthy rats intracellular Ca2+ store 0.19, 0.38 and 0.76g/L XMLI can increase the content of Ca2+ in cardiomyocytes. This effect of 0.38g/L XMLI can be slightly inhibited by 40μmol/L verapamil (inhibition rate is 20%), however, this effect of 0.19 and 0.76g/L XMLI cannot be inhibited by 40μmol/L verapamil.
Peng et al. 2003[23] hypoxia-reoxygenated cardiomyocytes of rats cardiomyocyte [Ca2+]i; MDA; SOD XMLI can increase [Ca2+]i in hypoxia and hypoxia-reoxygenated myocardium, increase SOD level and decrease MDA level. And this effect cannot be inhibited by verapamil.
Liu et al. 2017[24] alcoholic cardiomyopathy rats myocardial tissue microstructure changes; indicators of cardiac Doppler ultrasound; CTGF XMLI can reduce CTGF expression and ECM collagen deposition in rats with alcoholic cardiomyopathy.
Qi et al. 2017[3] HF mice with TAC surgery;
H9C2 cells (rat cardiomyocytes)		 LVPW thickness; EF; FS; phosphorylation of ERK1/2, AKT, and GSK3β; expression of GATA4 in the nucleus XMLI can reduce the diastolic thickness of the LVPW, increase EF and FS. XMLI can inhibit the phosphorylation of ERK1/2, AKT, and GSK3β, subsequently inhibiting protein expression of GATA4 in the nucleus.
Wu et al. 2009[25] pulmonary hypertension rats mean PAP; ET; NO XMLI can significantly reduce PAP while increasing plasma NO level and lowering plasma ET level.
Huang and Wu 2009[26] asphyxiating newborn rats CK; ET-1; HIF-1α; myocardial histopathological changes XMLI can reduce the expression of HIF-1α, reduce plasma ET-1 level, and alleviate myocardial hypoxia-ischemic injury.
Zhang et al. 2012[27] AS rats NO; ET; PGI2; TXA2 XMLI can significantly increase serum NO level and plasma PGI2, and significantly reduce plasma ET level in AS rats.
Sun and Zhang 2012[28] AS rats TC; TG; LDL-C; HDL-C XMLI can significantly reduce the levels of serum TC, TG and LDL-C and increase the level of HDL-C in AS rats.
Wu et al. 2002[29] healthy rats for preparing arrhythmia model survival time; the lethal dose of BaCI2 in rabbits; the rate of sinus rhythm conversion XMLI can significantly increase the lethal dose of BaCI2 in rabbits and prolong the survival time of rabbits. It prevents and reduces VPB, VT, and VF caused by BaCI2. It can also significantly improve the rate of sinus rhythm conversion.
Li et al. 2018[30] healthy rabbits for preparing atrial electrical remodeling model AERP XMLI can prevent the shortening of AERP200 and AERP150 after 6 hours of rapid pacing.

XMLI: Xinmailong Injection; ECG: electrocardiogram; CPK: creatine phosphokinase; LDH: lactate dehydrogenase; MDA: malondialdehyde; SOD: superoxide dismutase; GSH-PX: glutathione peroxidase; NO2−/NO3−: ratio of nitrite to nitrate; NCX: Na+/Ca2+ exchanger; ROS: reactive oxygen species; HO: heme oxygenase; iNOS: inducible nitric oxide synthase; ecNOS: endothelial constitutive nitric oxide synthase; CK-MB: creatine kinase-MB; NF-κB; nuclear factor-kappa B; TNF-α: tumor necrosis factor-α; HF: heart failure; LV: left ventricular; EF: ejection fraction; FS: fraction shortening; BNP: brain natriuretic peptide; cTnI: cardiac troponin I; LVPW: left ventricular posterior wall; MMP: matrix metalloproteinase; TIMPs: tissue inhibitors of matrix metalloproteinase; TGF-β1: transforming growth factor-β1; Ace: angiotensin-converting enzyme; Mas: proto-oncogene Mas; PI3K: phosphatidylinositol 3 kinase; AKT: protein kinase B; GSK3β: glycogen synthase kinase 3β; MAPK: mitogen-activated protein kinases; ERK1/2: extracellular regulated protein kinases 1/2; Atg7: autophagy-related gene 7; QTc: corrected QT; IL: interleukin; CTGF: connective tissue growth factor; ECM: extracellular matrix; TAC: transverse aortic coarctation; PAP: pulmonary artery pressure; ET: endothelin; NO: nitric oxide; HIF-1α: hypoxia-inducible factor-1α; AS: atherosclerosis; PGI2: prostacyclin 2; TXA2: thromboxane 2; TC: total cholesterol; TG: triglyceride; LDL-C: low density lipoprotein cholesterol; HDL-C: high density lipoprotein cholesterol; VPB: ventricular premature beat; VT: ventricular tachycardia; VF: ventricular fibrillation; AERP: atrial effective refractory period.