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andrographolide/atrofi

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Intervertebral disc degeneration (IDD) is a multifactorial disease with few efficacious clinical drugs, which has been demonstrated to be associated with nucleus pulposus (NP) cells apoptosis and degeneration of the extracellular matrix (ECM). Interleukin (IL)‑1β, a common proinflammatory cytokine,

Andrographolide prevents human nucleus pulposus cells against degeneration by inhibiting the NF-κB pathway.

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Intervertebral disc degeneration (IDD) is among the most common spinal disorders, pathologically characterized by excessive cell apoptosis and production of proinflammatory factors. Pharmacological targeting of nucleus pulposus (NP) degeneration may hold promise in IDD therapy, but it is limited by

Andrographolide enhances proliferation and prevents dedifferentiation of rabbit articular chondrocytes: an in vitro study.

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As the main active constituent of Andrographis paniculata that was applied in treatment of many diseases including inflammation in ancient China, andrographolide (ANDRO) was found to facilitate reduction of edema and analgesia in arthritis. This suggested that ANDRO may be promising

Andrographolide attenuates choroidal neovascularization by inhibiting the HIF-1α/VEGF signaling pathway

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Choroidal neovascularization (CNV), a characteristic of wet age-related macular degeneration (AMD), leads to severe vision loss amongst the elderly in the developed countries. Currently, the premier treatment for AMD is anti-VEGF therapy, which has limited efficacy, and is still controversial.
Abdominal aortic aneurysm (AAA), characterized by exuberant inflammation and tissue deterioration, is a common aortic disease associated with a high mortality rate. There is currently no established pharmacological therapy to treat this progressive disease. Andrographolide (Andro), a major bioactive

Andrographolide Alleviates Acute Brain Injury in a Rat Model of Traumatic Brain Injury: Possible Involvement of Inflammatory Signaling.

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Neuroinflammation plays an important role in secondary injury after traumatic brain injury (TBI). Andrographolide (Andro), a diterpenoid lactone isolated from Andrographis paniculata, has been demonstrated to exhibit anti-inflammatory activity in neurodegenerative disorders. This study therefore
BACKGROUND Andrographolide, extracted from the leaves of Andrographis paniculata (Burm. f.) Nees (Acanthaceae), is a labdane diterpene lactone. It is widely reported to possess anti-inflammatory and antitumorigenic activities. Cerebral endothelial cells (CECs) play a crucial role in supporting the

Andrographolide ameliorates intracerebral hemorrhage induced secondary brain injury by inhibiting neuroinflammation induction.

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Microglia activation and neuroinflammation play important roles in intracerebral hemorrhage (ICH)-induced secondary brain injury (SBI). In this study, we attempted to investigate the potential effects of Andrographolide (Andro) on ICH-induced SBI and the possible mechanisms behind these effects.

Andrographolide alleviates parkinsonism in MPTP-PD mice via targeting DRP1-mediated mitochondrial fission.

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Accumulating evidences indicate that mitochondrial dynamics plays an important role in the progressive deterioration of dopaminergic neurons. Andrographolide, a clinically used drug, has been found to exert neuroprotective effects in several experimental models of neurological disease.
Multiple sclerosis (MS) is a chronic immune mediated disease and the progressive phase appears to have significant neurodegenerative mechanisms. The classification of the course of progressive MS (PMS) has been re-organized into categories of active vs. not active inflammatory disease
Cartilage erosion in degenerative joint diseases leads to lameness in affected horses. It has been reported that andrographolide from Andrographis paniculata inhibited cartilage matrix-degrading enzymes. This study aimed to explore whether this compound protects equine cartilage degradation in the
Osteoporosis is a bone disease that is associated with a decrease in bone mineral density, deterioration of bone microarchitecture and increased fracture risk. Currently, available treatments mainly focus on either inhibiting osteoclast function, such as administration of
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