Estrogen receptor‐β of microglia underlies sexual differentiation of neuronal protection via ginsenosides in mice brain

Lee, Seung-Yeop; Lee, Sion; Kim, Gyu-Lee; Rhee, Dong‐Kwon

doi:10.1111/cns.12842

Cited by 17 publications

(17 citation statements)

References 55 publications

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“…Moreover, 20(S)-Rg3 is more suitable for application in clinical medicine, such as a novel inhibitor of autophagy [15] or protecting INS-1 cell death from intermittent high glucose [16]. It also has been confirmed that 20(S)-Rg3 is a compound that has many pharmacological effects such as anticancer [17], inhibition of brain injury [18], and diabetic kidney injury resistance [19]. Thus, 20(S)-Rg3 therapy has now become a nontraditional therapy for diabetes and its complications treatment.…”

Section: Introductionmentioning

confidence: 96%

20(S)-Ginsenoside Rg3 Protects Kidney from Diabetic Kidney Disease via Renal Inflammation Depression in Diabetic Rats

Zhou

Sun

Yang

et al. 2020

Journal of Diabetes Research

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Rg3) has been shown to induce apoptosis by interfering with several signaling pathways. Furthermore, it has been reported to have anticancer and antidiabetic effects. In order to detect the protective effect of 20(S)-Rg3 on diabetic kidney disease (DKD), diabetic rat models which were established by administering high-sugar, high-fat diet combined with intraperitoneal injection of streptozotocin (STZ), and age-matched wild-type (WT) rat were given 20(S)-Rg3 for 12 weeks, with three groups: control group (normal adult rats with saline), diabetic group (diabetic rats with saline), and 20(S)-Rg3 treatment group (diabetic rats with 20(S)-Rg3 (10 mg/kg body weight/day)). The biochemical indicators and the changes in glomerular basement membrane and mesangial matrix were detected. TUNEL staining was used to detect glomerular and renal tubular cell apoptosis. Immunohistochemical staining was used to detect the expression of fibrosis factors and inflammation factors in rat kidney tissues. Through periodic acid-Schiff staining, we observed that the change in renal histology was improved and renal tubular epithelial cell apoptosis decreased significantly by treatment with 20(S)-Rg3. Plus, the urine protein decreased in the rats with the 20(S)-Rg3 treatment. Fasting blood glucose, creatinine, total cholesterol, and triglyceride levels in the 20(S)-Rg3 treatment group were all lower than those in the diabetic group. Mechanistically, 20(S)-Rg3 dramatically downregulated the expression of TGF-β1, NF-κB65, and TNF-α in the kidney. These resulted in a significant prevention of renal damage from the inflammation. The results of the current study suggest that 20(S)-Rg3 could potentially be used as a novel treatment against DKD.

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Section: Introductionmentioning

confidence: 96%

20(S)-Ginsenoside Rg3 Protects Kidney from Diabetic Kidney Disease via Renal Inflammation Depression in Diabetic Rats

Zhou

Sun

Yang

et al. 2020

Journal of Diabetes Research

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“…Primary microglia from male rats migrate faster than those from females and show phagocytic capacity in vitro. Furthermore, microglial density varies among different regions varies based on sex in mice at different stages throughout life …”

Section: Different Sexual Microglia and Interventions For Strokementioning

confidence: 99%

“…Furthermore, microglial density varies among different regions varies based on sex in mice at different stages throughout life. 38,39 It is widely accepted that males and females respond to stroke differently. Biological sex influences many variables that are important in stroke, such as general health condition, cerebrovascular status, symptomatology, and therapeutic response.…”

Section: Ifferent S E Xual MI Crog Lia and Interventi On S For S mentioning

confidence: 99%

Potential microglia‐based interventions for stroke

Huang

Yang

et al. 2020

CNS Neurosci Ther

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A large number of families worldwide suffer from the physical and mental burden posed by stroke. An increasing number of studies aimed at the prevention and treatment of stroke have been conducted. Specifically, manipulating the immune response to stroke is under intense investigation. Microglia are the principal immune cells in the brain and are the first line of defense against the pathophysiology induced by stroke. Increasing evidence has suggested that microglia play diverse roles that depend on dynamic interactions with neurons, astrocytes, and other neighboring cells both in the normal brain and under pathological conditions, including stroke. Moreover, there are dynamic alterations in microglial functions with respect to aging and sex differences in the human brain, which offer a deep understanding of the conditions of stroke patients of different ages and sex. Hence, we review the dynamic microglial reactions caused by aging, sex, and crosstalk with neighboring cells both in normal conditions and after stroke and relevant potential interventions.

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“…Microglia are sedentary immunomodulatory cells in our central nervous system (CNS) that play critical roles in host defence and immune surveillance and harmonize innate and adaptive immune responses, which involve antigen presentation, phagocytosis, cell proliferation, cell migration, and cytokine production . Under normal circumstances, microglial cells not only perform immune surveillance but also react to danger signals owing to distinct microglial phenotypes, including proinflammatory M1 and antiinflammatory M2 phenotypes . Activated microglial cells undergo morphological transformation to the M1 phenotype and then secrete proinflammatory cytokines, resulting in self‐perpetuating injury to neurons .…”

Section: Introductionmentioning

confidence: 99%

“…16,17 Under normal circumstances, microglial cells not only perform immune surveillance but also react to danger signals owing to distinct microglial phenotypes, including proinflammatory M1 and antiinflammatory M2 phenotypes. [18][19][20] Activated microglial cells undergo morphological transformation to the M1 phenotype and then secrete proinflammatory cytokines, resulting in self-perpetuating injury to neurons. 21,22 The other phenotype, the M2 phenotype, is neuroprotective and can promote recovery.…”

Section: Introductionmentioning

confidence: 99%

Rosiglitazone polarizes microglia and protects against pilocarpine‐induced status epilepticus

et al. 2019

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Aims Activated microglia have been found in the forebrains and hippocampi of temporal lobe epilepsy (TLE) patients and status epileptic (SE) animal models. The peroxisome proliferator‐activated receptor γ (PPAR γ) agonist rosiglitazone has been shown to prevent microglial activation. However, its role in pilocarpine‐induced status epilepticus remains unknown. We aimed to examine the effect of the PPAR γ agonist rosiglitazone in protecting against pilocarpine‐induced status epileptic resulting from over‐activation and to explore phenotypic changes in microglia as the underlying mechanism. Methods Male C57BL/6 mice were assigned to three groups: the control group, pilocarpine‐induced (SE) group, and rosiglitazone‐treated (SE+Rosi) group. Status epileptic mice were administered 300 mg/kg pilocarpine via intraperitoneal injection. SE+Rosi mice were administered rosiglitazone (0.1 mg/kg, i.p.) after SE. Flow cytometry, immunofluorescence staining, and quantitative real‐time PCR were used to examine the activation of and phenotypic changes in microglia in the brain and to evaluate neuroinflammation. Results We found that the expression of proinflammatory CD86 and iNOS was increased and that the expression of antiinflammatory CD206 and Arg‐1 was decreased in the brains of pilocarpine‐induced SE mice compared to control mice. The mRNA levels of proinflammatory and antiinflammatory cytokines were not significantly changed in the brain. Rosiglitazone treatment significantly inhibited the proinflammatory polarization of microglia and rescued neuron loss in the temporal lobe and hippocampi of the brain after SE. Conclusion Rosiglitazone reverses microglial polarization in the brains of SE mice and also affords neuroprotection against pilocarpine‐induced status epilepticus without inducing significant changes in brain inflammation.

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Estrogen receptor‐β of microglia underlies sexual differentiation of neuronal protection via ginsenosides in mice brain

Abstract: After S. pneumoniae infection in mice, particularly in female mice, Rb1-containing ginseng increased bacterial clearance and survival. These findings inform our understanding of the host immune response to pneumococcal meningitis.

Cited by 17 publications

References 55 publications

20(S)-Ginsenoside Rg3 Protects Kidney from Diabetic Kidney Disease via Renal Inflammation Depression in Diabetic Rats

20(S)-Ginsenoside Rg3 Protects Kidney from Diabetic Kidney Disease via Renal Inflammation Depression in Diabetic Rats

Potential microglia‐based interventions for stroke

Rosiglitazone polarizes microglia and protects against pilocarpine‐induced status epilepticus

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