Mingmu Xiaomeng Tablets Restore Autophagy and Alleviate Diabetic Retinopathy by Inhibiting PI3K/Akt/mTOR Signaling

Fang, Yu-Wei; Shi, Kangpei; Lü, Haining; Lü, Lin; Qiu, Bo

doi:10.3389/fphar.2021.632040

Cited by 11 publications

(6 citation statements)

References 53 publications

(47 reference statements)

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“…Some classical drugs are proved to be beneficial for retinal inflammation control. For example, the traditional Chinese medicine, Mingmu Xiaomeng tablets reduce serum levels of interleukin (IL)-1β, IL-4, IL-6, TNF-α, and VEGF ( Fang et al, 2021 ). Also, the vitamin thiamine confirms once more to be an effective agent in reducing diabetes-induced retinal damage ( Mazzeo et al, 2020 ).…”

Section: Treatment For Retinal Inflammation Through Mgmentioning

confidence: 99%

Regulations of Retinal Inflammation: Focusing on Müller Glia

Chen

Xia

Zeng

et al. 2022

Front. Cell Dev. Biol.

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Retinal inflammation underlies multiple prevalent retinal diseases. While microglia are one of the most studied cell types regarding retinal inflammation, growing evidence shows that Müller glia play critical roles in the regulation of retinal inflammation. Müller glia express various receptors for cytokines and release cytokines to regulate inflammation. Müller glia are part of the blood-retinal barrier and interact with microglia in the inflammatory responses. The unique metabolic features of Müller glia in the retina makes them vital for retinal homeostasis maintenance, regulating retinal inflammation by lipid metabolism, purine metabolism, iron metabolism, trophic factors, and antioxidants. miRNAs in Müller glia regulate inflammatory responses via different mechanisms and potentially regulate retinal regeneration. Novel therapies are explored targeting Müller glia for inflammatory retinal diseases treatment. Here we review new findings regarding the roles of Müller glia in retinal inflammation and discuss the related novel therapies for retinal diseases.

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Section: Treatment For Retinal Inflammation Through Mgmentioning

confidence: 99%

Regulations of Retinal Inflammation: Focusing on Müller Glia

Chen

Xia

Zeng

et al. 2022

Front. Cell Dev. Biol.

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“…In this study, a diabetes model of mice was established through feeding a high-fat–high-glucose diet and intraperitoneal injection of STZ. The results showed that BJ significantly inhibited the formation of acellular capillaries in the retina of model mice, reduced the expression of VEGF, and promoted the expression of ZO-1, thus hindering the development of DR. After we conferred with the relevant literature, calcium dobesilate (CAD) was selected as a positive drug in vivo experiments ( 27 , 28 ), which has antioxidant, free radical, and vascular protection effects. Many randomized controlled clinical trials have confirmed the efficacy and safety of CAD in the treatment of DR ( 29 ).…”

Section: Discussionmentioning

confidence: 99%

Bie-Jia-Ruan-Mai-Tang, a Chinese Medicine Formula, Inhibits Retinal Neovascularization in Diabetic Mice Through Inducing the Apoptosis of Retinal Vascular Endothelial Cells

Liu

Chen

et al. 2022

Front. Cardiovasc. Med.

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Proliferative diabetic retinopathy (PDR) is one of the main complications of diabetes, mainly caused by the aberrant proliferation of retinal vascular endothelial cells and the formation of new blood vessels. Traditional Chinese medicines possess great potential in the prevention and treatment of PDR. Bie-Jia-Ruan-Mai-Tang (BJ), a Chinese medicine formula, has a good therapeutic effect on PDR clinically; however, the mechanism of action involved remains unclear. Therefore, we investigated the effect of BJ on PDR through in vitro and in vivo experiments. A diabetic mouse model with PDR was established by feeding a high-fat–high-glucose diet combined with an intraperitoneal injection of streptozotocin (STZ), while high-glucose-exposed human retinal capillary endothelial cells (HRCECs) were employed to mimic PDR in vitro. The in vivo experiments indicated that BJ inhibited the formation of acellular capillaries, decreased the expression of VEGF, and increased the level of ZO-1 in diabetic mice retina. In vitro experiments showed that high glucose significantly promoted cell viability and proliferation. However, BJ inhibited cell proliferation by cycle arrest in the S phase, thus leading to apoptosis; it also increased the production of ROS, decreased the mitochondrial membrane potential, reduced the ATP production, and also reduced the expressions of p-PI3K, p-AKT, and Bcl-xL, but increased the expressions of Bax and p-NF-κB. These results suggest that BJ induces the apoptosis of HRCECs exposed to high glucose through activating the mitochondrial death pathway by decreasing the PI3K/AKT signaling and increasing the NF-κB signaling to inhibit the formation of acellular capillaries in the retina, thus impeding the development of PDR.

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“…204 STAT3 activation increased TNFα expression and promoted ZO-1 disintegration to injure blood-retinal barrier. 61 The activation of PI3K/AKT could mediate endothelial cells autophagy, 205 slow down vascular endothelial cell-mesenchymal transformation, 206 and improve visual impairment in DR. Therefore, inflammation aggravates the damage of blood-retinal barrier in DR patients and increases the risk of visual impairment and blindness (Figure 5).…”

Section: Visual Impairment and Risk Of Blindnessmentioning

confidence: 99%

Inflammation in diabetes complications: molecular mechanisms and therapeutic interventions

Zhao,

Hu,

Zhang

et al. 2024

MedComm

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At present, diabetes mellitus (DM) has been one of the most endangering healthy diseases. Current therapies contain controlling high blood sugar, reducing risk factors like obesity, hypertension, and so on; however, DM patients inevitably and eventually progress into different types of diabetes complications, resulting in poor quality of life. Unfortunately, the clear etiology and pathogenesis of diabetes complications have not been elucidated owing to intricate whole‐body systems. The immune system was responsible to regulate homeostasis by triggering or resolving inflammatory response, indicating it may be necessary to diabetes complications. In fact, previous studies have been shown inflammation plays multifunctional roles in the pathogenesis of diabetes complications and is attracting attention to be the meaningful therapeutic strategy. To this end, this review systematically concluded the current studies over the relationships of susceptible diabetes complications (e.g., diabetic cardiomyopathy, diabetic retinopathy, diabetic peripheral neuropathy, and diabetic nephropathy) and inflammation, ranging from immune cell response, cytokines interaction to pathomechanism of organ injury. Besides, we also summarized various therapeutic strategies to improve diabetes complications by target inflammation from special remedies to conventional lifestyle changes. This review will offer a panoramic insight into the mechanisms of diabetes complications from an inflammatory perspective and also discuss contemporary clinical interventions.

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Mingmu Xiaomeng Tablets Restore Autophagy and Alleviate Diabetic Retinopathy by Inhibiting PI3K/Akt/mTOR Signaling

Cited by 11 publications

References 53 publications

Regulations of Retinal Inflammation: Focusing on Müller Glia

Regulations of Retinal Inflammation: Focusing on Müller Glia

Bie-Jia-Ruan-Mai-Tang, a Chinese Medicine Formula, Inhibits Retinal Neovascularization in Diabetic Mice Through Inducing the Apoptosis of Retinal Vascular Endothelial Cells

Inflammation in diabetes complications: molecular mechanisms and therapeutic interventions

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