Ecotoxicology and environmental safety · 2025
Effects of tea polyphenols and tea polysaccharides on improving nonylphenol-induced depression-like behavior, monoamine neurotransmitter disorder, and neuronal pyroptosis.
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Zhang Yujie, Chen Jingting, Xu Jie, Yang Xiao, Wang Songhe, Zeng Yingxi, Liu Junni, Yu Jie
Аннотация
BACKGROUND: Exposure to nonylphenol (NP) has been linked to depressive-like behaviors, while tea consumption is associated with a reduced risk of depression. This study investigates and compares the effects of tea polyphenols (TPs) and tea polysaccharides (TPSs) in alleviating NP-induced depressive-like behaviors, focusing on neuronal apoptosis and disrupted monoamine neurotransmitter secretion.
METHODS: Thirty-two specific-pathogen-free male, Sprague-Dawley rats (age: 4 weeks) were randomly assigned to four groups: control (5 mL/kg corn oil), NP (40 mg/kg NP), NP+TPS (25 mg/kg TPS), and NP+TP (50 mg/kg TP) groups.
RESULTS: The NP+TP group exhibited a shorter latency period in the feeding test than the NP group. Both NP+TP and NP+TPS groups showed reduced immobility time in the tail suspension and forced swimming tests. NP accumulation in the midbrain and cortical tissues was lower in these two groups. Additionally, these groups showed an increased number of "pear-shaped" neurons and higher serum neurotransmitter levels. The NP+TP and NP+TPS groups also demonstrated increased expression of estrogen receptor β (ERβ), tryptophan hydroxylase (TPH1), tryptophan hydroxylase-2 (TPH2), 5-hydroxytryptamine (5-HT), and 5-hydroxyindoleacetic acid (5-HIAA) at both protein and gene levels. These two groups also showed a progressive increase in neuron counts, a more organized arrangement, and reduced nuclear staining intensity compared with the NP group. Moreover, their IL-1β and IL-18 levels were lower, along with a reduction in Iba-1-positive microglia. The neuronal apoptosis rate, number of apoptotic cells, and expression of apoptosis-related inflammatory proteins (NLRP3, GSDMD, and Caspase-1) were also decreased in the NP+TP and NP+TPS groups.
CONCLUSION: TP and TPS mitigate NP-induced depressive-like behaviors by significantly reducing neuronal apoptosis, normalizing monoamine neurotransmitter secretion, and alleviating neuroinflammation. These findings highlight the potential of these tea components as neuroprotective agents against environmental endocrine disruptor-induced depression.
METHODS: Thirty-two specific-pathogen-free male, Sprague-Dawley rats (age: 4 weeks) were randomly assigned to four groups: control (5 mL/kg corn oil), NP (40 mg/kg NP), NP+TPS (25 mg/kg TPS), and NP+TP (50 mg/kg TP) groups.
RESULTS: The NP+TP group exhibited a shorter latency period in the feeding test than the NP group. Both NP+TP and NP+TPS groups showed reduced immobility time in the tail suspension and forced swimming tests. NP accumulation in the midbrain and cortical tissues was lower in these two groups. Additionally, these groups showed an increased number of "pear-shaped" neurons and higher serum neurotransmitter levels. The NP+TP and NP+TPS groups also demonstrated increased expression of estrogen receptor β (ERβ), tryptophan hydroxylase (TPH1), tryptophan hydroxylase-2 (TPH2), 5-hydroxytryptamine (5-HT), and 5-hydroxyindoleacetic acid (5-HIAA) at both protein and gene levels. These two groups also showed a progressive increase in neuron counts, a more organized arrangement, and reduced nuclear staining intensity compared with the NP group. Moreover, their IL-1β and IL-18 levels were lower, along with a reduction in Iba-1-positive microglia. The neuronal apoptosis rate, number of apoptotic cells, and expression of apoptosis-related inflammatory proteins (NLRP3, GSDMD, and Caspase-1) were also decreased in the NP+TP and NP+TPS groups.
CONCLUSION: TP and TPS mitigate NP-induced depressive-like behaviors by significantly reducing neuronal apoptosis, normalizing monoamine neurotransmitter secretion, and alleviating neuroinflammation. These findings highlight the potential of these tea components as neuroprotective agents against environmental endocrine disruptor-induced depression.