Adjuvant rhubarb alleviates organs dysfunction and inhibits inflammation in heat stroke

Wan, Ying; Sun, Shi; Fu, Haiyan; Xu, Yin‐Kun; Liu, Qing; Yin, Jie; Wan, Bing

doi:10.3892/etm.2018.6327

Cited by 4 publications

(3 citation statements)

References 29 publications

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“…smoking and tiredness, may cause irreversible structural changes in a specific vascular territory 18 . However, the effect of cerebral ischemia on BBB, a diffusion barrier essential for maintenance of homeostasis and normal function of the central nervous system, has been broadly investigated 10 . In current study, we investigated the protection of the combination of TPG and TLPA on BBB by anti-inflammation, anti-oxidative stress and anti-apoptosis effects.…”

Section: Discussionmentioning

confidence: 99%

The effect and mechanism of combination of total paeony glycosides and total ligustici phenolic acids against focal cerebral ischemia

Feng

Song

et al. 2020

Sci Rep

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The root of Paeonia lactiflora Pall. (Chishao, CS) and Ligusticum chuanxiong Hort. (Chuanxiong, CX) were widely used as a drug pair in Chinese Medicine, and the combination of CS and CX showed a more significant inhibition on neuronal apoptosis in our previous study. In the present study, total paeony glycosides (TPGs) from CS and total ligustici phenolic acids (TLPAs) from CX were combined to evaluate the synergistic effects against focal cerebral ischemia both in vitro and in vivo. The combination of TPGs and TLPAs at 7:3 had the best anti-oxidative stress and anti-inflammatory effect on OGD-induced HUVEC. Additionally, the infarction area proportion and neuron apoptosis of rats by TPGs:TLPAs (7:3) was significantly lower than their alone in MCAO rats. Moreover, TPGs: TLPAs of 7:3 showed a more significant effect on decreasing the expression of MMP-2 and MMP-9, and increasing the protein expression or mRNA level of TIMP-1 than other combinations. The optimal ratio of TPGs and TLPAs at 7:3 could bring more remarkable protective effects against focal cerebral ischemia in MCAO rats by alleviating oxidative stress, inflammatory and neuronal apoptosis to protect the blood-brain barrier. Overall, the present study provided benefical evidence for clinical application of CS and CX as a "drug pair". As the third highest worldwide cause of mortality 1 , stroke has been treated using antithrombotic therapy 2 , anticoagulant therapy 3,4 , neuroprotective and vascular dilated therapy. Numerous studies have demonstrated that the severity of neuronal apoptosis was associated with neurofunction, indicating a crucial role in the prognosis of ischemic stroke sufferer 5. Early anti-inflammatory and anti-oxidative stress may promote apoptosis of nerve cells. Thus attenuating these potential damage of nerve cells in ischemic area will be an effective strategy in clinical application. Chinese medicine (CM) has been used to treat stroke for a long time. Many classical prescriptions for treating cerebral diseases, such as Xiao-xu-ming decoction 6 are still being commonly used in modern clinial both in China and in other countries 7,8. Paeonia lactiflora Pall. (Chinese name: Chishao, CS) has been used worldwide for centuries and reported to exhibit various pharmacological bioactivities including anticoagulation, cognition enhancement, immunoregulatory 9 and anticance 10 , antioxidative 11 , and antidiabetic properties 12. The ischemic stroke protection of Paeoniae Radix may be related to its anti-oxidative stress and improvement of brain microcirculation. Ligusticum chuanxiong Hort. (Chinese name: Chuanxiong, CX) which belongs to the Umbelliferae family, is a valuable medicinal herb used worldwide and has been used for the treatment of atherosclerosis, hypertension, angina pectoris, and anti-inflammatory via acilitating blood circulation and dispersing blood stasis 13. Our previous study revealed the combination of CS and CX exerted more remarkable protective effects than alone by attenuating ER-stress-dependent apoptotic signaling and...

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Section: Discussionmentioning

confidence: 99%

The effect and mechanism of combination of total paeony glycosides and total ligustici phenolic acids against focal cerebral ischemia

Feng

Song

et al. 2020

Sci Rep

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“…It was also found that 18 FDG was primarily aggregated in the kidneys, which is consistent with the increase observed in the creatinine levels of the mice. Earlier studies have investigated the pathogenesis of HS mainly in terms of systemic inflammation ( 54 ) or nervous system protection ( 55 ). The present study aimed to acquire a deeper understanding of the mechanisms underlying HS-induced AKI, which has been rarely studied and could provide novel insight.…”

Section: Discussionmentioning

confidence: 99%

Metabolomic profiling identifies a novel mechanism for heat stroke‑related acute kidney injury

Guo

et al. 2021

Mol Med Rep

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Heat stroke can induce a systemic inflammatory response, which may lead to multi-organ dysfunction including acute kidney injury (AKI) and electrolyte disturbances. To investigate the pathogenesis of heat stroke (HS)-related AKI, a mouse model of HS was induced by increasing the animal's core temperature to 41°C. Blood samples obtained from the tail vein were used to measure plasma glucose and creatinine levels. Micro-positron emission tomography-computed tomography (micro-PET/CT), H&E staining and transmission electron microscopy were conducted to examine metabolic and morphological changes in the mouse kidneys. Immunohistochemistry (IHC) and western blot analyses were performed to investigate the expression of apoptosis-inducing factor mitochondria-associated 2 (Aifm2), high-mobility group box 1 (HMGB1) and receptor for advanced glycosylation end products (RAGE). Liquid chromatography-mass spectrometry analysis was conducted to find differential metabolites and signaling pathways. The HS mouse model was built successfully, with significantly increased creatinine levels detected in the serum of HS mice compared with controls, whereas micro-PET/CT revealed active metabolism in the whole body of HS mice. H&E and TUNEL staining revealed that the kidneys of HS mice exhibited signs of hemorrhage and apoptosis. IHC and western blotting demonstrated significant upregulation of Aifm2, HMGB1 and RAGE in response to HS. Finally, 136 differential metabolites were screened out, and enrichment of the ‘biosynthesis of unsaturated fatty acids’ pathway was detected. HS-associated AKI is the renal manifestation of systemic inflammatory response syndrome, and may be triggered by the HMGB1/RAGE pathway. Metabolomics indicated increased adrenic acid, docosahexaenoic acid and eicosapentaenoic acid may serve as metabolic biomarkers for AKI in HS. The findings suggested that a correlation between the HMGB1/RAGE pathway and biosynthesis of unsaturated fatty acids may contribute to the progression of HS-related AKI.

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“…AKI often manifests as oliguria, electrolyte imbalance, and elevated creatinine (Cr) levels, and requires continuous renal replacement therapy (6,7). The mechanism underlying the occurrence of AKI in EHS is not yet fully understood and may include hyperthermia, hypoperfusion, systemic inflammatory response syndrome (SIRS), disseminated intravascular coagulation (DIC), and rhabdomyolysis (8)(9)(10)(11)(12). Thus, a stable animal model is particularly important if the pathogenesis of EHS-AKI is to be studied in-depth.…”

Section: Introductionmentioning

confidence: 99%

A mouse model of exertional heatstroke-related acute kidney injury

Song¹,

Li²,

Hu³

et al. 2022

Ann Transl Med

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Background: Acute kidney injury (AKI) is a common complication of exertional heat stroke (EHS) with a complex pathogenesis. We established a stable mouse model of EHS-related AKI (EHS-AKI).Methods: C57BL/6 male mice were divided into 6 groups: Saline Control group, Glycerol Control group, Saline + Sham heat exercise (SHE) group, Saline + Heat exercise (HE) group, Glycerol + SHE group, and Glycerol + HE group. Samples from the Saline Control group and the Glycerol Control group were taken 6 h after the intramuscular injection of saline (4 mL/kg) or glycerol (4 mL/kg) to provide a baseline for comparisons with the other 4 groups. The other 4 groups of mice started exercise 6 h after the intramuscular injection of saline or glycerol, and were sacrificed to collect samples after exercise. Finally, serum and the pathology of kidney and muscle tissues were quantified.Results: There were no differences in the creatinine (Cr), blood urea nitrogen (BUN), creatine kinase (CK), and myoglobin (MYO) levels, but the interleukin 6 (IL-6) level was more increased (P<0.05) in the Glycerol Control group than the Saline Control group at the baseline. The IL-6 levels of the Glycerol + HE group were also higher than those of the Saline + HE groups at 6 and 12 h (P<0.05). The Cr levels at 12 h and 1 day, the BUN levels at 6 h, 12 h, 1 day, and 2 days in the Glycerol+ HE group were higher than the baseline levels (P<0.05). And the renal pathological scores at 6 h, 12 h, 1 day, 2 days, or 3 days were 0.79, 1.29, 1.58, 0.85, and 0.77. However, there was only slight renal pathological injury in the Saline + HE group at 12 h, and 1 day, and the scores were 0.13, and 0.41. The CK level in each group all peaked at 6 h after exercise and higher than the baseline (P<0.05). However, there was no difference in the MYO levels of each group compared to the baseline. Conclusions:We established a stable mouse model of EHS-AKI by conducting a heat exercise after the intramuscular injection of glycerol. Our findings lay the foundation for follow-up clinical and basic research.

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Adjuvant rhubarb alleviates organs dysfunction and inhibits inflammation in heat stroke

Cited by 4 publications

References 29 publications

The effect and mechanism of combination of total paeony glycosides and total ligustici phenolic acids against focal cerebral ischemia

The effect and mechanism of combination of total paeony glycosides and total ligustici phenolic acids against focal cerebral ischemia

Metabolomic profiling identifies a novel mechanism for heat stroke‑related acute kidney injury

A mouse model of exertional heatstroke-related acute kidney injury

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