TABLE 2.

Effect of D‐galactose administration on cardiac oxidative stress and inflammation

Ref	Study model	Age	Dose (mg/kg/day)	Route	Duration	Intervention	Major findings	Interpretation
JCR Q2 IF:7.7 10	Wistar rats	200–220 g	150	SC	4 or 8 weeks	—	MDA↑; TNF‐α↑	D‐galactose‐induced ageing aggravated cardiac oxidative status in obese insulin‐resistant rats
JCR Q3 IF:3.4 11	Kunming mice	6–8 weeks	500	SC	60 days	PSP; 200, 400 mg/kg/day; 60 days; Ig	ROS, MDA↑——↓; SOD↓——↑	PSP attenuated D‐gal‐induced cardiac ageing via inhibiting oxidative stress
JCR Q3 IF:5.7 12	Wistar rats	200–220 g	150	SC	8 weeks (after 12 weeks to induce obese‐insulin‐resistant condition by eating a high‐fat diet)	HBOT; 100% oxygen (O2) with 250 L/min flow rate; 80 min; once daily for 14 days (after 8 weeks d‐gal injection)	MDA↑——↓; TNF‐α↑——↓	HBOT effectively alleviated cardiac dysfunction via attenuating mitochondrial dysfunction in pre‐diabetic rats
JCR Q4 IF:2.6 13	SD rats	8 weeks	150	——	8 weeks	AOF; 50, 100, 150 mg/kg/day; 10 weeks; orally	HO1 and Cu/ZN SOD↓——↑(50↔)	AOF negatively modulated the D‐galactose‐induced cardiac hypertrophy signalling mechanism to attenuate ventricular hypertrophy
JCR Q3 IF:2.9 22	ICR mice	10 weeks	120	IP	6 weeks	ITPL; 50 mg/kg, 100 mg/kg; 10 weeks (pretreated 4 weeks and then treated with D‐galactose for 6 weeks); Ig	MDA, NO↑——↓; SOD, GSH, GSH‐Px↓——↑	ITPL increased superoxide dismutase, glutathione peroxidase, and glutathione levels and reduced nitric oxide and malondialdehyde levels in the serum in oxidative damaged mice induced by D‐gal
JCR Q1 IF:4 24	Kunming mice	10 weeks	120	IP	6 weeks	Lactobacillus plantarum KSFY02; 1.0 × 109 CFU/kg; 10 weeks(pretreat 4 weeks and then 6 weeks during the D‐galactose injections); Ig	MDA, NO↑——↓; SOD, GSH, G SH‐Px↓——↑	LP‐KSFY02 effectively inhibited the decrease in organ indices caused by oxidative ageing and alleviated body tissue atrophy caused by D‐galactose
JCR Q4 IF:2.0 28	Wistar rats	180–220 g	150	——	8 weeks	Mangiferin; 50 mg/kg/day, 100 mg/kg/day; 8 weeks; Ig	MDA↑——↓; SOD, C AT↓——↑; IL‐1β, IL‐6, T NF‐α↑——↓	Mangiferin suppressed D‐gal‐induced cardiac ageing, ameliorated cardiac oxidative stress, inflammation and fibrosis possibly via inhibiting TGF‐β/p38/MK2 signalling pathway
JCR Q3 IF:3.6 29	Kunming mice	4 weeks	500	SC	4 weeks	Lactobacillus plantarum NJAU‐01; 107, 108, and 109 CFU/ml; 4 weeks; Ig	MDA↑——↓; T‐AOC, SOD, GSH‐PX, CAT↓——↑	L. plantarum NJAU‐01 alleviated the oxidative damage induced by D‐galactose to the body and the strain concentration are related to the antioxidant effect
JCR Q3 IF:3.6 30	Wistar rats	170–220 g	150	IP	8 weeks	Resveratrol, 1 mg/kg/day, 8 weeks, Ig; Calcitriol, 0.1 μg/kg/day, 8 weeks, IP; Resveratrol + calcitriol; 8 weeks	MDA↑——↓; Cu/ZN SOD, Mn‐SOD, CAT mRNA, A and CAT activity ↓——↑; SOD↔——↑	Co‐administration of resveratrol and vitamin D protected the heart against ageing‐induced damage by the modulation of hemodynamic parameters and antioxidant status of the heart
JCR Q3 IF:2.4 34	Kunming mice	7–8 weeks	200	SC	6 weeks	Pine nut protein hydrolysate (PNPH); 150 mg/kg, 300 mg/kg, and 1000 mg/kg; 6 weeks; Ig	MDA↑——↓, SOD↓——↑, GSH‐Px↓——↑(150↔)	PNPH had antioxidant and anti‐ageing activities in vivo. It could reduce the oxidative damage in heart of mice and inhibit lipid peroxidation, thereby delaying the ageing process of mice induced by D‐galactose
JCR Q3 IF:6.9 35	C57BL/6J	6 weeks	200	SC	10 weeks	4% H2 inhalation; 4% (v/v) H2 gas for 2 h; 10 weeks	MDA, LPO↑——↓	H2 prevented oxidative stress in D‐galactose‐induced ageing mice when administered by different routes
						H2‐rich water drinking; concentration of H2 is above 600 μmol/L and could be drunk freely; 10 weeks	LPO↑——↓
						H2‐rich saline injection; 0.1 ml/10 g bw/day; 10 weeks; IP	—
JCR Q2 IF:6.3 32	C57BL/6	6 weeks	150	IP	10 weeks	CQ; 5 mg/kg/day; 8 weeks (starting from the 3rd week of D‐Gal injection); IP	IL‐1α, IL‐1β, IL‐6↑——↓	CQ possessed antisenescence and cardioprotective properties, and that oxidative‐stress‐induced senescence was suppressed by AMPK/SIRT1 and autophagy mechanisms
JCR Q2 IF:5.3 33	C57BL/6J	8 weeks	200	SC	8 weeks	AOS; 50, 100, 150 mg/kg/day; 4 weeks (The last four weeks of the D‐gal injection); Ig	ROS, MDA↑——↓; p47‐phox, p67‐phox and gp91‐phox↑——↓	AOS alleviated D‐gal‐induced cardiac ageing via regulating myocardial mitochondria function and integrity in mice
JCR Q2 IF:4.1 36	Wistar rats	18 weeks	150	—	4 weeks	AOF; 100 mg/kg/day; orally administered ADMSCs; administered intravenously with ADMSCs of 107 cells	Rac‐1, Nox‐2↑——↓; HO‐1 and Cu/ZN SOD↓——↑ IkB↓——↑; p‐NF‐κB, p65, IL‐6↑——↓	Synergistic effects of AOF and ADMSCs together possessed therapeutic values against cardiac ageing induced by D‐gal
JCR Q2 IF:5.1 37	Wistarrats	130–150 g	200	IP	8 weeks	Zeaxanthin heneicosylate(ZH); 250 μg/kg; 4 weeks after 8 weeks d‐gal injection; orally	SOD↓—↑, iNOS↑——↓; IL‐6, NF‐κB↑——↓	ZH isolated from D. salina ameliorated age‐associated cardiac dysfunction in rats through the activation of retinoid receptors
JCR Q3 IF:5.1 38	C57BL/6J	—	150	IP	8 weeks	CDDO‐Im; 3 μmol/kg/day; 8 weeks; IP	MDA, NO, and PC↑——↓; CAT, SOD, GSH‐Px↓——↑; HO‐1, SOD‐1↓	Nrf2 activator CDDO‐Im effectively protected against D‐galactose‐induced cardiac ageing by inhibiting oxidative stress in Nrf2+/+ mice (wild‐type mice)
JCR Q2 IF: 6.6 39	ICR mice	6 weeks	120	IP	6 weeks	Antarctic Ice Microalgae Polysaccharides (AIMP); 50 mg/kg or 100 mg/kg; 6 weeks; Ig	MDA, NO↑——↓; SOD, GSH, GSH‐Px↓——↑	AIMP effectively inhibited oxidative damage in mice with D‐galactose‐induced oxidative damage
JCR Q2 IF:6.5 40	C57BL/6	8 weeks	50	SC	8 weeks	NaHS; 10, 50, 100 μmol/kg/day; 8 weeks; IP	ROS↑——↓; SOD, GPx, NO↓——↑; CSE↓——↑(10↔); CBS↔ ——↑(10↔)and 3‐MST↔ H2S↓——↑(10, 50↔)	NaHS treatment protected against D‐gal‐accelerated ageing by reducing oxidative stress and increasing eNOS expression and NO contents as well as increasing endogenous H2S production
JCR Q3 IF:1.9 71	Kunming mice	18–22 g	125	SC	10 weeks	Dendrobium officinale (DO); DO‐1 (DO juice with a dose of 1 g/kg), DO‐2 (DO Polysaccharide with a dose of 0.32 g/kg); 9 weeks(from ten days after injection of D‐gal); orally	NO↔, SOD↓——↑	DO had a marked anti‐ageing effect on the D‐galactose‐induced model of ageing

Abbreviation: Ig, intragastric administration; IP, intraperitoneal; SC, subcutaneous; ↑, indicators increased under the action of D‐galactose; ↓, indicators decreased under the action of D‐galactose; ↑——↓, indicators increased under the action of galactose and decreased under the intervention; ↓——↑, indicators decreased under the action of D‐galactose and increased under the intervention; ↔, there was no change in the indicators under D‐galactose or intervention; (↔), under the intervention treatment of this dose, the indicators did not reverse the change caused by D‐galactose; ↔——↑, the indicators did not change after D‐galactose administration, but increased after intervention; in addition to the special notes in brackets, the intervention works together with D‐galactose.