1.浙江中医药大学生命科学学院,浙江省杭州市滨江区滨文路548号,310053
2.黑龙江中医药大学
3.黑龙江中医药大学附属第一医院
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收稿:2025-03-20,
修回:2025-06-26,
纸质出版:2025-09-17
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高青,孙河,王丽媛等.基于NLRP3/Caspase-1/IL-1β信号通路探讨通窍明目Ⅳ号方含药血清对L-谷氨酸诱导R28细胞损伤的影响[J].中医杂志,2025,66(18):1925-1933.
高青,孙河,王丽媛等.基于NLRP3/Caspase-1/IL-1β信号通路探讨通窍明目Ⅳ号方含药血清对L-谷氨酸诱导R28细胞损伤的影响[J].中医杂志,2025,66(18):1925-1933. DOI: 10.13288/j.11-2166/r.2025.18.012.
目的
2
探究通窍明目Ⅳ号方对青光眼视神经损伤的可能保护机制。
方法
2
将通窍明目Ⅳ号方拆方为疏肝方、明目方。30只大鼠随机分为全方组、疏肝组、明目组、正常组、维生素B
12
组,每组6只。全方组给予通窍明目Ⅳ号方94.5 g/(kg·d)灌胃,疏肝组给予疏肝方40.5 g/(kg·d)灌胃,明目组给予明目方54.0 g/(kg·d)灌胃,正常组给予蒸馏水18.9 ml/(kg·d)灌胃,维生素B
12
组给予维生素B
12
50 μg/(kg·d)灌胃。每日灌胃1次,连续7天后腹主动脉采血,分离血清。视网膜前体细胞系R28细胞分为空白组、模型组、正常血清组、全方血清组、疏肝血清组、明目血清组、维生素B
12
血清组,每组3个复孔。除空白组外,其余各组使用L-谷氨酸诱导R28细胞损伤模型(采用筛选出的诱导浓度和时间)。造模后空白组和模型组不予血清干预;正常血清组去除培养基加入10%正常组血清;全方血清组、疏肝血清组、明目血清组去除培养基加入10%相应中药组血清;维生素B
12
血清组去除培养基加入10%维生素B
12
血清。各组细胞继续培养48 h后,采用CCK-8法检测细胞活力(包括细胞存活率、抑制率);PI/Hoechst双染法检测细胞凋亡,比较染色荧光强度平均值;荧光探针法检测活性氧簇(ROS)含量;免疫荧光法、Western Blot法、qRT-PCR法分别检测NOD样受体热蛋白结构域蛋白3/含半胱氨酸的天冬氨酸特异性蛋白酶1/白细胞介素1β(NLRP3/Caspase-1/IL-1β)信号通路相关蛋白
及mRNA表达。
结果
2
筛选出浓度20 mmol/L的L-谷氨酸处理细胞48 h以诱导细胞损伤模型。与空白组比较,模型组R28细胞存活率降低、细胞抑制率升高,PI/Hoechst染色细胞荧光强度平均值升高,细胞中ROS含量、NLRP3/Caspase-1/IL-1β相关蛋白及其mRNA表达亦升高(
P
<0.05)。与模型组比较,各药物血清干预组上述各指标均不同程度改善(
P
<0.05)。且全方血清组在降低抑制率、PI/Hoechst染色荧光强度平均值、ROS含量、NLRP3/Caspase-1/IL-1β相关蛋白及其mRNA表达优于维生素B
12
血清组(
P
<0.05)。全方血清组、疏肝血清组PI/Hoechst染色荧光强度平均值低于明目血清组(
P
<0.05)。全方血清组
NLRP3、
凋亡相关斑点样蛋白(
ASC
)
、Caspase
-
1、IL
-
1β
mRNA表达均低于疏肝血清组、明目血清组(
P
<0.05)。
结论
2
通窍明目Ⅳ号方可能通过抑制NLRP3/Caspase-1/IL-1β信号通路,减轻程序性细胞坏死,从而有效缓解视网膜神经元凋亡,达到视神经保护的作用。
Objective
2
To explore the protective mechanism of
Tongqiao Mingmu IV Formula
(通窍明目Ⅳ号方) on glaucoma-induced optic nerve damage.
Methods
2
Tongqiao Mingmu IV Formula
was divided into
Shugan Formula
(疏肝方) and
Mingmu Formula
(明目方). Thirty rats were randomly assigned to whole formula group, Shugan
group, Mingmu
group, normal group, and vitamin B
12
group, with five rats in each group. The whole formula group received 94.5 g/(kg·d) of
Tongqiao Mingmu IV Formula
by gavage; Shugan group received 40.5 g/(kg·d) of
Shugan Formula
by gavage; Mingmu
group received 54.0 g/(kg·d) of
Mingmu Formula
by gavage; the control group received 18.9 ml/(kg·d) of distilled water by gavage; and the vitamin B
12
group received 50 μg/(kg·d) of vitamin B
12
by gavage. Administer oral gavage once daily for 7 consecutive days, then collect blood from the abdominal aorta and isolate serum. R28 retinal precursor cell lines were divided into blank group, model group, normal serum group, whole formula serum group, Sh
ugan serum group, Mingmu serum group, and vitamin B
12
serum group, with three replicate wells per group. Except for the blank group, all other groups employed L-glutamate to induce R28 cell damage using optimized induction concentrations and durations. After modeling, the blank group and model group received no serum intervention; the normal serum group had its medium removed and replaced with 10% normal serum; the whole formula serum group, Shugan serum group, and Mingmu serum group had their medium removed and replaced with 10% serum from the corresponding herbal formula group; the vitamin B
12
serum group had its medium removed and replaced with 10% vitamin B
12
serum. After 48 hours of continued culture, cell viability including survival rate and inhibition rate was assessed using the CCK-8 assay; apoptosis rates were determined via PI/Hoechst dual staining, comparing mean fluorescence intensities; reactive oxygen species (ROS) levels were measured using fluorescent probes; immunofluorescence, Western Blot, and qRT-PCR were used to detect the expression of proteins and mRNA related to the NOD-like receptor protein 3 (NLRP3)/Caspase-1/IL-1β signaling pathway.
Results
2
Cells were treated with 20 mmol/L L-glutamate for 48 hours to induce a cellular injury model. Compared with the blank group, the model group exhibited decreased R28 cell viability, increased cell inhibition rate, elevated average fluorescence intensity of PI/Hoechst staining, and increased levels of cellular ROS, NLRP3/Caspase-1/IL-1β-related proteins, and their mRNA expression (
P
<0.05). Compared with the model group, all serum intervention groups showed varying degrees of improvement in the aforementioned indicators (
P
<0.05). The whole formula serum group demonstrated superior effectiveness to the vitamin B
12
serum group in reducing inhibition rates, mean PI/Hoechst staining fluorescence intensity, ROS levels, and mRNA expression of NLRP3/Ca
spase-1/IL-1β-related proteins (
P
<0.05). The mean PI/Hoechst staining fluorescence intensity in whole formula serum group and Shugan serum group was lower than that in the Mingmu serum group (
P
<0.05).
NLRP3
,
Apoptosis
-
Related Speck
-
Like Protein
(
ASC
),
Caspase
-
1
, and
IL
-
1β
mRNA in the whole formula serum group was lower than that in both Shugan serum group and Mingmu serum group (
P
<0.05).
Conclusion
2
Tongqiao Mingmu IV Formula
may alleviate programmed cell necrosis by inhibiting the NLRP3/Caspase-1/IL-1β signaling pathway, thereby effectively reducing retinal neuronal apoptosis and achieving optic nerve protection.
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