高糖因素减弱七氟烷预处理心肌保护作用与HIF-1α/LDHA信号通路的关系

doi:10.3877/cma.j.issn.2095-1221.2026.04.004

目的

探讨高糖因素减弱七氟烷预处理对大鼠心肌细胞保护效应的机制与缺氧诱导因子-1α （HIF-1α）/乳酸脱氢酶A （LDHA）信号通路的关系。

方法

采用随机数字表法将H9c2细胞分为8组：对照组（N+Con组）、缺氧复氧组（N+H/R组）、七氟烷预处理组（N+SPC组）、高糖对照组（H+Con组）、高糖-缺氧复氧组（H+H/R组）、高糖七氟烷预处理组（H+SPC组）、高糖七氟烷预处理+HIF-1α激动剂组（H+SPC+D组）、高糖七氟烷预处理+HIF-1α激动剂+LDHA抑制剂组（H+SPC+D+A组）。CCK-8法检测心肌细胞活力；微板法检测培养液LDH水平；WST-8法检测乳酸水平；化学发光法检测ATP水平；ELISA检测糖酵解关键酶含量；Annexin V/PI双染法联合流式细胞术检测细胞凋亡率、荧光探针法检测线粒体膜电位，蛋白质印迹法检测HIF-1α、LDHA表达水平。多组间比较采用ANOVA单因素方差分析，组间两两比较采用Tukey's多重比较。

结果

与N+SPC组相比，H+SPC组细胞活力[（70.12 ± 3.81）%比（86.66 ± 5.48）%]、乳酸水平[（5.36 ± 0.18）比（6.94 ± 0.45）mmol/L]、ATP水平[（88.90 ± 17.33比172.88 ± 26.83） μmol/L]、线粒体膜电位（0.55 ± 0.11比0.78 ± 0.08）、细胞HK、PFK1、PK活性[（72.43 ± 8.77）比（134.23 ± 8.84）U/mL、（104.62 ± 10.65）比（213.30 ± 12.36）U/mL、（92.87 ± 5.14）比（251.67 ± 14.45）U/mL]、HIF-1α （0.54 ± 0.01比0.94 ± 0.04）和LDHA表达（0.69 ± 0.02比1.07 ± 0.04）均降低，培养液LDH水平[（315.12 ± 25.22）比（122.87 ± 8.03）U/L]和细胞凋亡率[（21.42 ± 2.11）%比（10.92 ± 0.69）%]均升高（P均< 0.05）；与H+SPC组相比，H+SPC+D组细胞活力[（83.72 ± 4.55）%比（70.12 ± 3.81）%]、乳酸水平[（6.40 ± 0.42）比（5.36 ± 0.18）mmol/L]、ATP水平[（165.62 ± 24.28）比（88.90 ± 17.33）μmol/L]、线粒体膜电位（0.82 ± 0.05比0.55 ± 0.11）、细胞HK、PFK1、PK活性[（122.34 ± 8.74）比（72.43 ± 8.77）U/mL、（192.45 ± 20.98）比（104.62 ± 10.65） U/mL、（208.76 ± 32.65）比（92.87 ± 5.14）U/mL]，HIF-1α （0.80 ± 0.03比0.54 ± 0.01）和LDHA表达（0.87 ± 0.04比0.69 ± 0.02）均升高，培养液LDH水平[（154.33 ± 26.85）比（315.12 ± 25.22）U/L]和细胞凋亡率[（15.43 ± 1.07）%比（21.42 ± 2.11）%]均降低（P均< 0.05）；与H+SPC+D组相比，H+SPC+D+A组细胞活力[（68.43 ± 3.20）%比（83.72 ± 4.55）%]、乳酸水平[（5.03 ± 0.12）比（6.40 ± 0.42）mmol/L]、ATP水平[（79.54 ± 19.22）比（165.62 ± 24.28） μmol/L]、线粒体膜电位（0.57 ± 0.05比0.82 ± 0.05）、细胞HK、PFK1、PK活性[（66.83 ± 6.91）比（122.34 ± 8.74） U/mL、（77.83 ± 5.94）比（192.45 ± 20.98）U/mL、（132.80 ± 3.53）比（208.76 ± 32.65）U/mL]，HIF-1α表达（0.35 ± 0.02比0.80 ± 0.03）和LDHA （0.45 ± 0.02比0.87 ± 0.04）均降低，培养液LDH水平[（264.96 ± 13.46）比（154.33 ± 26.85）U/L]和细胞凋亡率[（19.83 ± 0.23）%比（15.43 ± 1.07）%]均升高（P均< 0.05）。

结论

高糖因素减弱七氟烷预处理对大鼠心肌细胞保护效应的机制可能与抑制HIF-1α/LDHA信号通路活性有关。

关键词: 高糖, H9c2细胞, 缺氧/复氧损伤, 缺氧诱导因子1α, 乳酸脱氢酶A

Objective

To investigate whether the mechanism by which high glucose weaken the protective effect of sevoflurane pretreatment on rat cardiomyocytes is related to the HIF-1α/LDHA signaling pathway.

Methods

H9c2 cardiomyocytes were randomly divided into 8 groups using a random number table, and named control group (N+Con group), hypoxia-reoxygenation group (N+H/R group), sevoflurane preconditioning group (N+SPC group), high glucose control group (H+Con group), high glucose-hypoxia-reoxygenation group (H+H/R group), high glucose sevoflurane preconditioning group (H+SPC group), high glucose sevoflurane preconditioning + HIF-1α agonist group (H+SPC+D group), and high glucose sevoflurane preconditioning + HIF-1α agonist + LDHA inhibitor group (H+SPC+D+A group). Cell viability of cardiomyocytes was assessed using the CCK-8 assay. Lactate dehydrogenase (LDH) levels in the culture medium were measured via the microplate method. Lactate levels were determined using the WST-8 assay. ATP levels were detected by chemiluminescence assay. The levels of key glycolytic enzymes were quantified using ELISA. Apoptosis rate was evaluated by flow cytometry, and mitochondrial membrane potential was measured using a fluorescent probe. The expression levels of HIF-1α and LDHA were detected by western blotting. Comparisons among multiple groups were performed using one-way ANOVA, and pairwise comparisons between groups were conducted using Tukey's multiple comparison test.

Results

Compared with the N+SPC group, the H+SPC group showed decreases in cell viability [(70.12 ± 3.81)%vs (86.66 ± 5.48)%], lactate level [(5.36 ± 0.18) vs (6.94 ± 0.45) mmol/L], ATP level [(88.90 ± 17.33) vs (172.88 ± 26.83) μmol/L], mitochondrial membrane potential (0.55 ± 0.11 vs 0.78 ± 0.08), the activities of HK, PFK1, and PK [(72.43 ± 8.77) vs (134.23 ± 8.84) U/mL, (104.62 ± 10.65) vs (213.30 ± 12.36) U/mL, (92.87 ± 5.14) vs (251.67 ± 14.45) U/mL], the expression of HIF-1α (0.54 ± 0.01 vs 0.94 ± 0.04) and LDHA (0.69 ± 0.02 vs 1.07 ± 0.04) were decreased in the H+SPC group, while the LDH level in culture medium [(315.12 ± 25.22) vs (122.87 ± 8.03) U/L ] and apoptosis rate were increased [(21.42 ± 2.11)% vs (10.92 ± 0.69)%]. All differences were statistically significant (all P < 0.05). Compared with the H+SPC group, the cell viability [(83.72 ± 4.55)%vs (70.12 ± 3.81)%], lactate level [(6.40 ± 0.42) vs (5.36 ± 0.18) mmol/L], ATP level [(165.62 ± 24.28) vs (88.90 ± 17.33) μmol/L], mitochondrial membrane potential (0.82 ± 0.05 vs 0.55 ± 0.11), the activities of HK, PFK1, and PK [(122.34 ± 8.74 vs 72.43 ± 8.77) U/mL, (192.45 ± 20.98) vs (104.62 ± 10.65) U/mL, (208.76 ± 32.65) vs (92.87 ± 5.14) U/mL], the expression of HIF-1α (0.80 ± 0.03 vs 0.54 ± 0.01) and LDHA (0.87 ± 0.04 vs 0.69 ± 0.02) were increased in the H+SPC+D group, whereas culture medium LDH level [(154.33 ± 26.85) vs (315.12 ± 25.22) U/L ] and apoptosis rate [(15.43 ± 1.07)% vs (21.42 ± 2.11)%] were decreased. All differences were statistically significant (all P < 0.05). Compared with the H+SPC+D group, the cell viability [(68.43 ± 3.20)% vs (83.72 ± 4.55)%], lactate level [(5.03 ± 0.12) vs (6.40 ± 0.42) mmol/L], ATP level [(79.54 ± 19.22) vs (165.62 ± 24.28) μmol/L], mitochondrial membrane potential (0.57 ± 0.05 vs 0.82 ± 0.05), the activities of HK, PFK1, and PK [(66.83 ± 6.91) vs (122.34 ± 8.74) U/mL, (77.83 ± 5.94) vs (192.45 ± 20.98) U/mL, (132.80 ± 3.53) vs (208.76 ± 32.65) U/mL], the expression of HIF-1α (0.35 ± 0.02 vs 0.80 ± 0.03) and LDHA (0.45 ± 0.02 vs 0.87 ± 0.04) were decreased in the H+SPC+D+A group, while culture medium LDH level [(264.96 ± 13.46) vs (154.33 ± 26.85)U/L] and apoptosis rate [(19.83 ± 0.23)%vs (15.43 ± 1.07)%] were increased. All differences were statistically significant (all P < 0.05).

Conclusion

The mechanism by which high glucose attenuates the protective effect of sevoflurane preconditioning on rat cardiomyocytes may be related to the inhibition of HIF-1α/LDHA signaling pathway activity.

Key words: High glucose, H9c2 cells, Hypoxia/reoxygenation, Hypoxia inducible factor 1α, Lactate dehydrogenase A

图1 药物浓度筛选注：^*P < 0.05；^**P < 0.01；^***P < 0.001

图2 荧光倒置显微镜下观察H9c2细胞（JC-1染色，×200）注：SPC提高红绿色荧光强度的比值

图3 Annexin V/PI双染法联合流式细胞术检测细胞凋亡率

表1 各组细胞各项指标的比较（n = 3,

± s）

分组	细胞活力（%）	培养液LDH水平（U/L）	乳酸水平（mmol/L）	ATP水平（μmol/L）	凋亡率（%）	线粒体膜电位
N+Con组	100.03 ± 4.67	103.82 ± 14.08	3.75 ± 0.43	266.74 ± 26.08	5.11 ± 1.01	1.21 ± 0.02
N+H/R组	71.23 ± 4.23^a	275.96 ± 12.32^a	5.93 ± 0.19^a	86.61 ± 18.72^a	21.69 ± 0.37^a	0.54 ± 0.04^a
N+SPC组	86.66 ± 5.48^b	122.87 ± 8.03^b	6.94 ± 0.45^ab	172.88 ± 26.83^ab	10.92 ± 0.69^ab	0.78 ± 0.08^ab
H+Con组	91.15 ± 4.32^b	252.15 ± 24.19^abc	3.58 ± 0.33^bc	247.63 ± 21.45^abc	8.33 ± 0.07^abc	0.94 ± 0.02^ab
H+H/R组	65.74 ± 7.35^acd	367.52 ± 43.63^abcd	5.33 ± 0.22^abcd	38.59 ± 22.99^abcd	25.12 ± 0.46^abcd	0.46 ± 0.02^acd
H+SPC组	70.12 ± 3.81^acd	315.12 ± 25.22^abcde	5.36 ± 0.18^abcd	88.90 ± 17.33^acde	21.42 ± 2.11^acde	0.55 ± 0.11^acd
H+SPC+D组	83.72 ± 4.55^abef	154.33 ± 26.85^abdef	6.40 ± 0.42^abcdef	165.62 ± 24.28^abdef	15.43 ± 1.07^abcdef	0.82 ± 0.05^abef
H+SPC+D+A组	68.43 ± 3.20^acdg	264.96 ± 13.46^aceg	5.03 ± 0.12^abcdg	79.54 ± 19.22^acdeg	19.83 ± 0.23^acdeg	0.57 ± 0.05^acdg
F值	21.211	32.012	125.517	173.711	221.412	40.473
P值	< 0.001	< 0.001	< 0.001	< 0.001	< 0.001	< 0.001

表1 各组细胞各项指标的比较（n = 3,

± s）

分组	细胞活力（%）	培养液LDH水平（U/L）	乳酸水平（mmol/L）	ATP水平（μmol/L）	凋亡率（%）	线粒体膜电位
N+Con组	100.03 ± 4.67	103.82 ± 14.08	3.75 ± 0.43	266.74 ± 26.08	5.11 ± 1.01	1.21 ± 0.02
N+H/R组	71.23 ± 4.23^a	275.96 ± 12.32^a	5.93 ± 0.19^a	86.61 ± 18.72^a	21.69 ± 0.37^a	0.54 ± 0.04^a
N+SPC组	86.66 ± 5.48^b	122.87 ± 8.03^b	6.94 ± 0.45^ab	172.88 ± 26.83^ab	10.92 ± 0.69^ab	0.78 ± 0.08^ab
H+Con组	91.15 ± 4.32^b	252.15 ± 24.19^abc	3.58 ± 0.33^bc	247.63 ± 21.45^abc	8.33 ± 0.07^abc	0.94 ± 0.02^ab
H+H/R组	65.74 ± 7.35^acd	367.52 ± 43.63^abcd	5.33 ± 0.22^abcd	38.59 ± 22.99^abcd	25.12 ± 0.46^abcd	0.46 ± 0.02^acd
H+SPC组	70.12 ± 3.81^acd	315.12 ± 25.22^abcde	5.36 ± 0.18^abcd	88.90 ± 17.33^acde	21.42 ± 2.11^acde	0.55 ± 0.11^acd
H+SPC+D组	83.72 ± 4.55^abef	154.33 ± 26.85^abdef	6.40 ± 0.42^abcdef	165.62 ± 24.28^abdef	15.43 ± 1.07^abcdef	0.82 ± 0.05^abef
H+SPC+D+A组	68.43 ± 3.20^acdg	264.96 ± 13.46^aceg	5.03 ± 0.12^abcdg	79.54 ± 19.22^acdeg	19.83 ± 0.23^acdeg	0.57 ± 0.05^acdg
F值	21.211	32.012	125.517	173.711	221.412	40.473
P值	< 0.001	< 0.001	< 0.001	< 0.001	< 0.001	< 0.001

表2 各组H9C2细胞糖酵解关键酶水平的比较（n = 3，

± s）

分组	HK （U/mL）	PFK1 （U/mL）	PK （U/mL）
N+Con组	48.69 ± 4.00	79.38 ± 20.17	83.38 ± 8.63
N+H/R组	93.99 ± 4.59^a	148.81 ± 17.94^a	130.75 ± 3.18^a
N+SPC组	134.23 ± 8.84^ab	213.30 ± 12.36^ab	251.67 ± 14.45^ab
H+Con组	47.11 ± 4.51^bc	84.13 ± 13.24^bc	84.12 ± 7.71^bc
H+H/R组	57.71 ± 7.92^bcd	85.79 ± 12.67^bc	91.45 ± 5.03^bc
H+SPC组	72.43 ± 8.77^abcde	104.62 ± 10.65^abc	92.87 ± 5.14^bc
H+SPC+D组	122.34 ± 8.74^abcdef	192.45 ± 20.98^abdef	208.76 ± 32.65^abcdef
H+SPC+D+A组	66.83 ± 6.91^abcdg	77.83 ± 5.94^bcfg	132.80 ± 3.53^acdefg
F值	198.708	118.502	237.397
P值	< 0.001	< 0.001	< 0.001

表2 各组H9C2细胞糖酵解关键酶水平的比较（n = 3，

± s）

分组	HK （U/mL）	PFK1 （U/mL）	PK （U/mL）
N+Con组	48.69 ± 4.00	79.38 ± 20.17	83.38 ± 8.63
N+H/R组	93.99 ± 4.59^a	148.81 ± 17.94^a	130.75 ± 3.18^a
N+SPC组	134.23 ± 8.84^ab	213.30 ± 12.36^ab	251.67 ± 14.45^ab
H+Con组	47.11 ± 4.51^bc	84.13 ± 13.24^bc	84.12 ± 7.71^bc
H+H/R组	57.71 ± 7.92^bcd	85.79 ± 12.67^bc	91.45 ± 5.03^bc
H+SPC组	72.43 ± 8.77^abcde	104.62 ± 10.65^abc	92.87 ± 5.14^bc
H+SPC+D组	122.34 ± 8.74^abcdef	192.45 ± 20.98^abdef	208.76 ± 32.65^abcdef
H+SPC+D+A组	66.83 ± 6.91^abcdg	77.83 ± 5.94^bcfg	132.80 ± 3.53^acdefg
F值	198.708	118.502	237.397
P值	< 0.001	< 0.001	< 0.001

图4 Western blot检测HIF-1α和LDHA蛋白表达注：与N+Con组比较，^aP < 0.05；与N+H/R组比较，^bP < 0.05；与N+SPC组比较，^cP < 0.05；与H+Con组比较，^dP < 0.05；与H+H/R组比较，^eP < 0.05；与H+SPC组比较，^fP < 0.05；与H+SPC+D组比较，^gP < 0.05

1	Rooney MR, He JH, Salpea P, et al. Global and regional prediabetes prevalence: updates for 2024 and projections for 2050[J]. Diabetes Care, 2025,48(11):e142-e144.
2	Rajan N, Duggan EW, Abdelmalak BB, et al. Society for ambulatory anesthesia updated consensus statement on perioperative blood glucose management in adult patients with diabetes mellitus undergoing ambulatory surgery[J]. Anesth Analg, 2024, 139(3):459-477.
3	Hou T, Ma H, Wang H, et al. Sevoflurane preconditioning attenuates hypoxia/reoxygenation injury of H9c2 cardiomyocytes by activation of the HIF-1/PDK-1 pathway[J]. PeerJ. 2020, 8:e10603.
4	Hu B, Tian T, Hao PP, et al. The protective effect of sevoflurane conditionings against myocardial ischemia/reperfusion injury: a systematic review and meta-analysis of preclinical trials in in-vivo models[J]. Front Cardiovasc Med, 2022, 9:841654.
5	Gao S, Wang R, Dong S, et al. Inactivation of topk caused by hyperglycemia blocks diabetic heart sensitivity to sevoflurane postconditioning by impairing the PTEN/PI3K/Akt signaling[J]. Oxid Med Cell Longev, 2021, 2021:6657529.
6	Yu J, He J, Yang W, et al. Diabetes impairs the protective effects of sevoflurane postconditioning in the myocardium subjected to ischemia/ reperfusion injury in rats: important role of Drp1[J]. BMC Cardiovasc Disord, 2021, 21(1):96.
7	Yang L, Xie P, Wu J, et al. Deferoxamine treatment combined with sevoflurane postconditioning attenuates myocardial ischemia-reperfusion injury by restoring HIF-1/BNIP3-mediated mitochondrial autophagy in gk rats[J]. Front Pharmacol, 2020, 19, 11:6.
8	杜文涛. LDHA对心肌缺血再灌注损伤中细胞凋亡作用影响的研究[D]. 石家庄：河北医科大学, 2018.
9	Yi Y, Wu MY, Chen KT, et al. LDHA-mediated glycolysis in stria vascularis endothelial cells regulates macrophages function through CX3CL1-CX3CR1 pathway in noise-induced oxidative stress[J]. Cell Death Dis, 2025, 16(1):65.
10	Xu F, Liu Y, Zhu X, et al. Protective effects and mechanisms of vaccarin on vascular endothelial dysfunction in diabetic angiopathy[J]. Int J Mol Sci, 2019, 20(18):4587.
11	Ruan Z, Wang S, Yu W, et al. LncRNA NEAT1 aggravates diabetic myocardial ischemia-reperfusion injury through regulating PINK1 by targeting miR-27b[J]. Int J Cardiol, 2019, 286:136.
12	方媛,郭统帅,吴岳,等.高糖通过诱导自噬障碍促进心肌细胞H9c2凋亡[J/OL]. 中华细胞与干细胞杂志（电子版）, 2018, 8(3):134-139.
13	王蕊,郝翠君,周金才,等.二氢杨梅素对高糖诱导的H9c2心肌细胞损伤的影响[J/OL]. 中华细胞与干细胞杂志（电子版）, 2022, 9(3): 160-165.
14	侯天亮,杨龙,马海平,等.高糖因素减弱七氟烷后处理心肌保护效应与HIF-1α/MCT4信号通路的关系：细胞实验[J]. 中华麻醉学杂志, 2025, 45(11):1433-1438.
15	Semenza GL. Oxygen sensing, homeostasis, and disease[J]. N Engl J Med, 2011, 365(6):537-547.
16	Ma H, Hou T, Wu J, et al. Sevoflurane postconditioning attenuates cardiomyocytes hypoxia/reoxygenation injury via PI3K/AKT pathway mediated HIF-1α to regulate the mitochondrial dynamic balance[J]. BMC Cardiovasc Disord, 2024, 24(1):280.
17	Liao Y, Yang L, Guo C, et al. Echinacoside targets the HIF-1α/LDHA axis to modulate A1/A2 astrocyte differentiation and promote glial scar repair following ischemic stroke[J]. J Ethnopharmacol, 2025, 353(Pt B):120375.
18	Zhong L, Li J, Yu J, et al. Anemarrhena asphodeloides Bunge total saponins ameliorate diabetic cardiomyopathy by modifying the PI3K/AKT/HIF-1α pathway to restore glycolytic metabolism[J]. J Ethnopharmacol, 2024, 319(Pt 3):117250.
19	Ma H, Li Y, Hou T, et al. Sevoflurane postconditioning attenuates hypoxia/reoxygenation injury of cardiomyocytes under high glucose by regulating HIF-1α/MIF/AMPK pathway[J]. Front Pharmacol, 2021, 11:624809.
20	Osis G, Traylor AM, Black LM, et al. Expression of Lactate Dehydrogenase A and B isoforms in the mouse kidney[J]. Am J Physiol Renal Physiol, 2021, 320(5):F706-F718.
21	史文花, 陈玉倩, 张永红,等.青蒿素通过HIF-1α/LDHA通路抑制糖酵解改善肺血管重塑[J]. 实用医学杂志, 2025, 41(1):15-22.

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[3]	张秀杨, 张龙飞, 陈世远, 高涌. 缺氧诱导因子1α介导单羧酸转运蛋白1表达参与短链脂肪酸对肠道缺氧保护作用的研究[J/OL]. 中华普通外科学文献(电子版), 2023, 17(01): 18-23.
[4]	罗育春, 罗育连, 徐园园, 唐清珠. 薯蓣皂甙元通过miR-145-5p/KLF5/HIF-1α轴抑制结直肠癌细胞增殖、迁移和侵袭[J/OL]. 中华普通外科学文献(电子版), 2021, 15(03): 178-184.
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The relationship between the weakened myocardial protective effect of sevoflurane pretreatment by high glucose factors and the HIF-1α/LDHA signaling pathway

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The relationship between the weakened myocardial protective effect of sevoflurane pretreatment by high glucose factors and the HIF-1α/LDHA signaling pathway