Frontiers in pharmacology · 2026
Protective effects of a commercial total flavonoid preparation from Puerariae Lobatae Radix on exhaustive exercise-induced liver injury in mice.
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Zhou Zhenmao, Yang Fan, Zhao Chengkun, Qiu Xiangchen, Yuan Ding
Аннотация
OBJECTIVE: This study investigated the protective effects of a commercial total flavonoid preparation derived from Puerariae Lobatae Radix on exhaustive exercise-induced liver injury in mice, with a focus on oxidative stress, inflammatory responses, and NF-κB-related signaling.
METHODS: A mouse model of exhaustive exercise-induced liver injury was established by exhaustive swimming. Mice were assigned to a normal control group, an exercise model group, a silymarin-treated group, and low-, medium-, and high-dose total flavonoid preparation groups. Liver function, histopathological alterations, oxidative stress-related parameters, inflammatory mediators, and NF-κB-related signaling proteins were evaluated after 4 weeks of treatment.
RESULTS: Exhaustive exercise induced marked liver injury, as evidenced by elevated serum ALT and AST levels, histopathological damage, aggravated oxidative stress, and increased inflammatory responses. In the exercise model group, serum GSH decreased from 155.77 ± 9.32 to 71.64 ± 4.20 μmol/L, hepatic MDA increased from 3.80 ± 1.50 to 8.34 ± 1.58 nmol/mg protein, hepatic GSH decreased from 1.43 ± 0.05 to 1.00 ± 0.07 nmol/mg protein, and hepatic SOD decreased from 0.92 ± 0.56 to 0.33 ± 0.21 U/mg protein. Treatment with the tested total flavonoid preparation attenuated these alterations, with the medium-dose group showing the most consistent effects, including restoration of serum GSH to 135.84 ± 10.49 μmol/L, reduction of hepatic MDA to 4.07 ± 0.68 nmol/mg protein, increase of hepatic GSH to 1.35 ± 0.05 nmol/mg protein, and increase of hepatic SOD to 0.86 ± 0.07 U/mg protein. The preparation also reduced inflammatory mediator expression and modulated NF-κB-related signaling, as reflected by decreased p-IKKα and increased p-IκBα expression.
CONCLUSION: The tested total flavonoid preparation attenuated exhaustive exercise-induced liver injury in mice. Its protective effects were associated with reduced oxidative stress, suppression of inflammatory responses, and modulation of NF-κB-related signaling, supporting its potential value in preventing exercise-related hepatic stress.
METHODS: A mouse model of exhaustive exercise-induced liver injury was established by exhaustive swimming. Mice were assigned to a normal control group, an exercise model group, a silymarin-treated group, and low-, medium-, and high-dose total flavonoid preparation groups. Liver function, histopathological alterations, oxidative stress-related parameters, inflammatory mediators, and NF-κB-related signaling proteins were evaluated after 4 weeks of treatment.
RESULTS: Exhaustive exercise induced marked liver injury, as evidenced by elevated serum ALT and AST levels, histopathological damage, aggravated oxidative stress, and increased inflammatory responses. In the exercise model group, serum GSH decreased from 155.77 ± 9.32 to 71.64 ± 4.20 μmol/L, hepatic MDA increased from 3.80 ± 1.50 to 8.34 ± 1.58 nmol/mg protein, hepatic GSH decreased from 1.43 ± 0.05 to 1.00 ± 0.07 nmol/mg protein, and hepatic SOD decreased from 0.92 ± 0.56 to 0.33 ± 0.21 U/mg protein. Treatment with the tested total flavonoid preparation attenuated these alterations, with the medium-dose group showing the most consistent effects, including restoration of serum GSH to 135.84 ± 10.49 μmol/L, reduction of hepatic MDA to 4.07 ± 0.68 nmol/mg protein, increase of hepatic GSH to 1.35 ± 0.05 nmol/mg protein, and increase of hepatic SOD to 0.86 ± 0.07 U/mg protein. The preparation also reduced inflammatory mediator expression and modulated NF-κB-related signaling, as reflected by decreased p-IKKα and increased p-IκBα expression.
CONCLUSION: The tested total flavonoid preparation attenuated exhaustive exercise-induced liver injury in mice. Its protective effects were associated with reduced oxidative stress, suppression of inflammatory responses, and modulation of NF-κB-related signaling, supporting its potential value in preventing exercise-related hepatic stress.