“To Live is to suffer, to survive is to find some meaning in the suffering” – Friederich Nietzsche


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Minocycline (Minocin) is an antibiotic, part of the group of antibiotics known as tetracyclines, and has been long used successfully as an antibiotic in treating acne and some sexually transmitted diseases. Recently, it has been discovered that minocycline can exert a variety of biological actions that are independent of its anti-microbial activity, including anti-inflammatory, and anti-apoptotic (cell death) actions as well as neuroprotection.


Minocycline is now sometimes used to treat the signs and symptoms of other conditions not associated with infection but, instead, associated with neuroinflammation. Neuroinflammation is inflammation of nervous tissue in the peripheral or central nervous system which occurs in response to a variety of triggers including trauma, infection, toxins, or auto-immune processes. 


Neuroinflammation plays a central role in chronic pain as well as other conditions including rheumatoid arthritis, fibromyalgia, depression, PTSD, multiple sclerosis, Parkinson’s Disease, Alzheimer Disease, brain and spinal cord injuries, chronic traumatic encephalopathy (CTE), stroke and schizophrenia.


The following is a review of current research evaluating the potential role for minocycline in the management of chronic pain and other symptoms as manifest in a variety of medical conditions.






Central Sensitization

See also:


Neurobiology of Pain

Neuropathic (Nerve) Pain

Neurobiology of Opioids


Opioid Tolerances

Medications for Pain

Gabapentin (Neurontin) & Pregabalin (Lyrica)

Toll-Like Receptor Antagonists (TLR-4)

Traumatic Brain Injury


 Definitions and Terms Related to Pain

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Minocycline has recently emerged as an effective agent regarding neuroprotection, an effect that has been confirmed in experimental models of traumatic brain injury and spinal cord injury (SCI), neuropathic pain and of several neurodegenerative conditions including Parkinson’s and Huntington’s Chorea, amyotrophic lateral sclerosis (ALS), Alzheimer’s disease, and multiple sclerosis.


These pre-clinical animal studies led to the evaluation of minocycline in clinical trials in patients with neuronal disease, where it has shown promising neuroprotective benefits. The growing interest in minocycline has led to evaluations of its therapeutic benefits for many other diseases, such as arachnoiditis, rheumatoid arthritis, inflammatory bowel disease, diabetes, cardiac ischaemia and human immunodeficiency virus (HIV) infection.


As a result of these studies, various mechanisms have been proposed that may be involved in minocycline’s anti-inflammatory, immunomodulatory and neuroprotective effects and will be reviewed further below. However, minocycline’ therapeutic benefits are believed to be derived through inhibition of glial cell activation and suppression of neuroinflammation.

See: Neuroinflammation


Minocycline – Rhematoid Arthritis (RA)

Minocycline has been shown to provide clinically useful anti-inflammatory properties in patients with rheumatoid arthritis, superior to the placebo. Early studies concluded that minocycline might be beneficial in patients with rheumatoid arthritis for inhibition of cartilage degradation, especially when administered early in the course of the disease or in patients with only mild disease. Minocycline demonstrated beneficial effects with respect to joint swelling and/or tenderness, laboratory parameters and patient self-assessments. A meta-analysis in 2003 confirmed these beneficial effects.


Despite these early promising results, a 2011 study concluded that the weak anti-inflammatory properties of minocycline are easily surpassed by many other anti-inflammatory agents. Nevertheless, the potential benefit of minocycline in RA and osteoarthritis treatment are still under investigation.


Inflammation is a complex biological response that is basic to how the body addresses injury and infection to eliminate the initial cause of cell injury and repair tissues. While acute inflammation is normally a beneficial response, chronic inflammation often results from an inappropriate immune response that can lead to tissue damage and ultimately tissue destruction. Inflammation in the nervous system or “neuroinflammation,” especially when prolonged, can be particularly harmful. While inflammation per se may not cause disease, it contributes importantly to the process of disease in both the peripheral and central nervous systems. Treatment of neuroinflammation may significantly impact the progression and symptomatic manifestation of those conditions associated with neuroinflammation.


 Neuroinflammation is implicated in:

  1. Pain
  2. Opioid tolerance
  3. Fibromyalgia
  4. Reward Deficiency Syndrome (RDS)
  5. Traumatic brain injury (TBI)
  6. Arachnoiditis
  7. Depression
  8. Multiple Sclerosis
  9. Alzheimer disease
  10. Parkinson disease
  11. Autism Spectrum Disorder


(1). Pain and Neuroinflammation

Until recently, opioids and medications such as gabapentin (Neurontin), pregabalin (Lyrica) and duloxetine (Cymbalta) have been the conventional approach to reduce pain by their action on transduction and transmission in neurons, which likely accounts for the limited success in controlling chronic pain and its  progression. This “nerve-based” view fails to address the fact that initiation and maintenance of neuropathic pain depends to a great extent on non-nerve cells such as spinal microglia and astrocytes, together with elements of the peripheral immune system.

Chronic pain is maintained in part by central sensitization, a process involving adaptations at the nerve synapses and increased responsiveness to painful stimul in the pain pathways. Central sensitization is  driven by neuroinflammation in the peripheral and central nervous system. Neuroinflammation, characterized by the activation of glial cells such as microglia and astrocytes in the spinal cord and brain, leads to the release of proinflammatory cytokines and chemokines. These cytokines and chemokines impact  nerves, inducing hyperalgesia and allodynia, and their sustained release in the central nervous system promotes chronic widespread pain affecting multiple body sites. Thus, understanding how neuroinflammation in the peripheral and central nervous system drives widespread chronic pain via central sensitization has gained recent attention for its importance in understanding and treating chronic pain and other conditions. See Treatment of Neuroinflammation (below).

See Central Sensitization

(2). Opioid Tolerance and Neuroinflammation

Classical neuron-centered concepts about tolerance, such as internalization of opioid receptors, upregulation of N-methyl-D-aspartate (NMDA) receptor function, or downregulation of glutamate transporter activity only partially explain the phenomenon of tolerance. Recent evidence confirms that glial activation and upregulation of inflammatory mediators in the central nervous system play pivotal roles in neuropathic pain and opioid tolerance.

(3). Fibromyalgia and Neuroinflammation

Coming soon…

(4). Reward Deficiency Syndrome and Neuroinflammation

See: Reward Deficiency Syndrome and Chronic Pain

(5). Traumatic Brain Injury and Neuroinflammation

See: Traumatic Brain Injury

(6). Arachnoiditis

See: Arachnoiditis

(7). Depression and Neuroinflammation

Coming soon… 

Treatment of Neuroinflammation

Early studies suggest that medications or supplements that reduce neuroinflammation by inhibiting glial activation and/or stabilizing mast cells may reduce the development of chronic nerve pain or reduce the severity of existing nerve pain. They may also be useful in suppressing the development of opioid tolerance. Various inhibitors of glial activation that are being evaluated for clinical use in the managment of chronic pain include minocycline, a tetracycline-class antibiotic, low dose naltrexone, palmi
toylethanolamide (PEA)
and Acetyl-L-carnitine. There is some evidence as well that gabapentin may inhibit glial cell activation as another mechanism of action responsible for its effectiveness in treating nerve pain. Furthermore, there may be a role for antioxidants and NRF2 activators as well in the management of chronic nerve pain related to glial cell activation.


At this time, the following agents are considered good candidates for treating neuroinflammation through stabilization and/or suppression of glial cells and mast cells:


  1. Palmitoylethanolamide (PEA)
  2. Cannabidiol (CBD)
  3. Minocycline – Recognized as a microglia inhibitor
  4. Low-dose naltrexone
  5. DHEA – Early/weak evidence for benefit in depression and regulation of the blood-brain barrier


Understanding Neuroinflammation

Understanding communication between the nervous system and the immune system is fundamental to understand neuroinflammation. Immune cell-derived inflammatory molecules regulate of host responses to inflammation. Although these molecules can originate from various non-neuronal (non-nerve) cells, their most important sources are immune cells: microglia and mast cells, together with astrocytes and possibly also oligodendrocytes. Understanding neuroinflammation also requires an appreciation that non-neuronal cell—cell interactions, between both glia and mast cells and glia themselves, are an integral part of the inflammation process. Within this context the mast cell occupies a key niche in orchestrating the inflammatory process, from initiation to prolongation.


Normal, optimal inflammatory responses and physiological levels of inflammatory mediators are beneficial and protect the body as they remove unwanted waste materials and repair damaged tissues. As such, the initial, acute inflammatory response is protective, and lipid mediators such as eicosanoids (prostaglandins and leukotrienes produced from the essential fatty acid arachidonic acid) play critical roles in the initial response, with interactions between prostaglandins, leukotrienes and pro-inflammatory cytokines amplifying inflammation.

Normally, these altered and reactive immune cells diminish their activity within 10–14 days after injury and the inflammatory response ceases. However, in some cases, this neuroinflammation continues and becomes chronic, leading to many of the manifestations of nerve pain, or “neuropathic” pain, such as hyperalgesia, allodynia and peripheral and central sensitization, all of which are characterized by a magnification of pain experience.


The Players in Neuroinflammation

The process of neuroinflammation can be understood on a (1) structural level, including the blood-brain barrier (BBB), on a (2) cellular level including immune cells such as mast cells, microglia, astrocytes and oligodendrocytes or on a (3) chemical level including cytokines, chemokines and others.


Neuroinflammation and the Blood-Brain Barrier (BBB)

In normal physiological conditions, the blood-brain barrier (BBB) prevents entry of most drugs, chemicals, toxins and peripheral blood cells into the brain and central nervous system. The BBB is an extensive network of endothelial cells (ECs) in brain capillaries together with neurons and glial cells, including microglia, that form a neurovascular unit (NVU). The communication between these cells maintains a proper environment for brain function.


The integrity of the BBB which prevents”inappropriate” molecules from entering the central nervous system and brain is dependent on the maintenance of “tight junctions,” where the cells of the blood vessel interface with adjoining cells. Changes in the interactions between blood vessel endothelium and microglia are associated with a variety of inflammation-related diseases where BBB permeability is compromised. Evidence indicates that activated microglia modulate expression of tight junctions, which are essential for BBB integrity and function. On the other hand, the endothelium can in turn regulate the state of microglial activation.


Trauma and its associated stress induces a local inflammatory response causing disruption and dysfunction of the BBB increasing its permeability. This results in the infiltration of peripheral immune and inflammatory cells such as neutrophils, monocytes, mast cells (see below), and T cells into the brain. These cells become “activated,” immediately releasing inflammatory proteins called cytokines and chemokines within hours post-injury. These mast cell-derived inflammatory mediators further increase blood brain barrier (BBB) permeability and activate localized brain-based immune glial cells such as microglia and astrocytes (see below). When activated, microglia and astrocytes increase production of similar inflammatory cytokines. Furthermore, all of these inflammatory mediators increase vascular permeability and increase escape and recruitment of immune and inflammatory cells at the site of injury. When the integrity of the BBB is compromised through inflammation or injury, there is increased permeability of the BBB, allowing for increased introduction of inflammatory chemicals, drugs and toxins to
enter the central nervous system (CNS)  – spinal cord and brain.


Although loss of BBB integrity is associated with several neuropathological disorders, treatments that improve or stabilise the BBB are scarce. A 2017 study suggests that dehydroepiandrosterone sulfate (DHEAS) supports the integrity of the BBB and DHEA has shown evidence for benefit in the treatmemt of depression. At this time, one focus of treatment of impaired BBB integrity lies in the stabilization of glial cells and mast cells.


The Blood Brain Barrier and the Intestinal Epithelial Barrier (IEB)

A growing body of evidence demonstrates that the integrity of the BBB is linked to the integrity of the intestinal epithelial barrier (IEB), the analogous structure to the BBB in the gut. In turn, the integrity of the IEB is linked to the gut microbiome, the populati0n of microbes in the intestinal tract, Disruption of the IEB leads to a condition called “leaky gut syndrome,” in which a disruption of the tight junctions of the cells lining the gut wall allows for the pathologic migration of agents within the gut into the blood and systemic circulation. These agents include bacterial products and dietary antigens which trigger an immune response causing the release of pro-inflammatory chemicals. This in turn contributes to the condition of systemic inflammation which is tied into neuroinflammation, and the potential development of a number of disease states. The gut microbiome appears to be a significant factor contributing to the maintenance or the breakdown of the IEB and the gut microbiome is influenced and modified by a number of factors including stress and drugs, in particular NSAIDs and opioids. Leaky gut syndrome is believed to be associated with many pathological states, especially stress-related disorders including IBS, inflammatory bowel disease (Crohn’s and ulcerative colitis), fibromyalgia, depression, headaches and other chronic pain-related conditions.

See: Leaky Gut (Coming soon… )



Neuroinflammation and Glial Cells

Glial cells are cells found in the central and peripheral nervous system.  They function to maintain balance in nerve and neurotransmitter activity, they form myelin (the coating of some nerve cells), and provide support and protection for neurons (nerve cells). Glial cells are derived from the immune system, the most common of which are microglia cells and astrocytes. Glia cells provide a supportive matrix for nerve cells, supplying nutrients and oxygen and aid in the repair of damaged cells. However, when activated, glial cells also are important in the evolution and maintenance of chronic nerve pain through the release of peptides known as cytokines that are pro-inflammatory, triggering chronic pain. They may play a role in opioid function including opioid-induced hyperalgesia and opioid tolerance. It is believed that pathologic glial cell activation plays a significant role in the evolution of fibromyalgia pain, central sensitization and other chronic pain syndromes.


Following activation, glia cells release pro-inflammatory cytokines/chemokines including:

(1) Tumor necrosis factor (TNF)

(2) Interleukin-1beta (IL-1β)

(3) Interleukin-6 (IL-6)

(4) Interleukin-8 (IL-8)

(5) Chemokine (C–C motif) ligand 2 (CCL-2), also known as monocyte chemoattractant protein 1 (MCP-1)

(6) Brain-derived neurotrophic factor (BDNF)

(7) Nerve growth factor (NGF)

(8) Glutamate

(9) Substance P (SP)

Neuroinflammation and Mast Cells

Glial cells participate in inflammation not only directly, but also in to response to molecular mediators produced by other immune system-derived cells, both blood-borne (dendritic cells, lymphocytes, neutrophils), and tissue-resident (mast cells). Mast cell are an important signaling link between the peripheral immune system and the brain in an inflammatory setting. Due to their widespread tissue presence near blood vessels and surfaces exposed to the environment, mast cells function as environmental “sensors” to communicate physiological and/or immune responses. Mast cells detect and respond to changes in environmental temperature and barometric pressure and are believed to play a role in the increased perception of pain associated with changes in weather.


Mast cells are manufactured in the bone marrow and enter the circulation and then into peripheral tissues including connective tissue cells and mucosal cells. They maintain broad tissue distribution, often close to blood vessels and near boundaries between the body’s external environment and the internal milieu, such as skin, mucosa of lungs and digestive tract, and in mouth, eye conjunctiva, and nose. Mast cells also found in the nervous system, including meningeal tissures that surround the brain, brain tissue, and nerve sleeves. They are integral in allergic reactions and anaphylactic shock, stress,  mood disorders, inflammatory pain, chronic and neuropathic pain and acute and chronic neurodegenerative disorders.

Mast cells are found in tissues innervated by small caliber sensory nerve fibers (A-delta and C-fibers responsible for pain transmission that extend from the periphery to the spinal cord an
d brain), in meninges, and apposing cerebral blood vessels. Mast cell’s key role in the inflammatory process, when activated, is to rapidly release granules (degranulation) of bioactive chemicals, pro-inflammatory mediators such as cytokines and others into the surrounding tissues. Degranulation is triggered by direct injury (physical or chemical), stimulation of immune receptors (such as IgE in allergies) or by activated complement proteins. More than 50 mediators are known and their expression by mast cells is complex and determined to a large extent by tissue location. Additionally, mast cell-derived chemoattractants recruit other immune cells including eosinophils, monocytes, and neutrophils, and can induce T cell activation, proliferation, and cytokine secretion.

As such, it is clear that glial cells and mast cells play major roles in neuroinflammatiom through their release of chemically active protein mediators that impact tissues and stimulate pain, acutely and chronically. Current research is focusing on medications and other agents that can stabilize glial cells and mast cells, suppress their release of mediators and thereby reduce the development and/or maintenance of chronic pain.

Neuroinflammation and Oligodendrocytes

Oligodendrocytes, the myelin-producing cells of the central nervous system (CNS), may also participate in the pain process. In addition to their production of myelin, oligodendrocytes support nerve function and long-term integrity. Oligodendrocyte damage/dysfunction leads to spinal nerve axon pathology and the induction/maintenance of increased pain sensitivity. Also, like glial cells and mast cells, they produce and respond to chemokines/cytokines that modulate CNS immune responses and interact with microglia.   In the case of multiple sclerosis (MS), for example, autoimmune inflammation driven by invading peripheral immune cells leads to injury/degeneration of oligodendrocytes and neurons, and contributes to the neuropathic pain often experienced by MS patients.

New Frontiers – Resolving Inflammation

The resolution of neuroinflammation has previously been considered a passive process. Recent research, however, has identified mediators with the capacity to actively resolve inflammation, endogenous agents called resolvins, protectins & maresins, that are involved with the process of shutting down neuroinflammation. It is hoped that in the future the means of harnessing these agents for therapeutic purposes will become available. What is believed at this time, however, is that production of these agents may be promoted by low dose aspirin and omega-3 essential fatty acids while NSAIDs may inhibit their production.

Coming Soon…



Minocycline – Overviews

  1. Critical data-based re-evaluation of minocycline as a putative specific microglia inhibitor. – PubMed – NCBI- 2017
  2. Minocycline – far beyond an antibiotic – 2013
  3. Minocycline (Minocin) – American College of Rheumatology – 2017
  4. Mycoplasmal Infections in Chronic Illnesses – Fibromyalgia and Chronic Fatigue Syndromes, Gulf War Illness, HIV-AIDS and Rheumatoid Arthritis – 1999

Minocycline – Acne

  1. Minocycline for acne vulgaris – Efficacy and safety 2012


Minocycline – Adverse Effects

  1. Minocycline-induced transient depersonalization – A case report – 2019


Minocycline – Central Sensitization

  1. Minocycline attenuates mechanical allodynia and central sensitization following peripheral second-degree burn injury. 2010 – PubMed – NCBI
  2. Neuropeptides and Microglial Activation in Inflammation, Pain, and Neurodegenerative Diseases – 2017

Minocycline – DPN

  1. Minocycline attenuates the development of diabetic neuropathic pain: possible anti-inflammatory and anti-oxidant mechanisms. – PubMed – NCBI 2011


Minocycline – Endocannabinoid System

  1. Coadministration of indomethacin and minocycline attenuates established paclitaxel-induced neuropathic thermal hyperalgesia – Involvement of cannabinoid CB1 receptors – 2015


Minocycline – Gastrointestinal (GI) Disease

  1. Neuroanatomy of lower gastrointest
    inal pain disorders – 2014


 Minocycline – Macular Degeneration

  1. Minocycline counter-regulates pro-inflammatory microglia responses in the retina and protects from degeneration – 2015


Minocycline – Neurobiology

  1. A novel role of minocycline: attenuating morphine antinociceptive tolerance by inhibition of p38 MAPK in the activated spinal microglia. – PubMed – NCBI
  2. Communicating systems in the body – how microbiota and microglia cooperate – 2017
  3. Critical data-based re-evaluation of minocycline as a putative specific microglia inhibitor – 2016
  4. Critical data-based re-evaluation of minocycline as a putative specific microglia inhibitor. – PubMed – NCBI- 2017
  5. Critical data-based re-evaluation of minocycline as a putative specific microglia inhibitor. 2016 – PubMed – NCBI
  6. Evidence for brain glial activation in chronic pain patients – 2015
  7. Exploring the neuroimmunopharmacology of opioids – an integrative review of mechanisms of central immune signaling and their implications for opioid analgesia – 2011
  8. Microglia and CNS Interleukin-1 – Beyond Immunological Concepts – 2018
  9. Minocycline blocks lipopolysaccharide induced hyperalgesia by suppression of microglia but not astrocytes – 2015
  10. Minocycline Provides Neuroprotection Against N-Methyl-d-aspartate Neurotoxicity by Inhibiting Microglia – 2001
  11. Minocycline reduces chronic microglial activation after brain trauma but increases neurodegeneration – 2018
  12. Minocycline targets multiple secondary injury mechanisms in traumatic spinal cord injury
  13. Minocycline, a microglial inhibitor, blocks spinal CCL2-induced heat hyperalgesia and augmentation of glutamatergic transmission in substantia gelatinosa neurons – 2014
  14. Minocycline, a Tetracycline Derivative, Is Neuroprotective against Excitotoxicity by Inhibiting Activation and Proliferation of Microglia – 2001
  15. Minocycline, a Tetracycline Derivative, Is Neuroprotective against Excitotoxicity by Inhibiting Activation and Proliferation of Microglia
  16. Multiple neuroprotective mechanisms of minocycline in autoimmune CNS inflammation. 2007 – PubMed – NCBI
  17. Neuropeptides and Microglial Activation in Inflammation, Pain, and Neurodegenerative Diseases – 2017
  18. Pathological pain and the neuroimmune interface – 2014
  19. Prolonged Minocycline Treatment Impairs Motor Neuronal Survival and Glial Function in Organotypic Rat Spinal Cord Cultures – 2013
  20. The brain’s best friend – microglial neurotoxicity revisited. – 2013
  21. The Importance of Therapeutic Time Window in the Treatment of Traumatic Brain Injury – 2019


Minocycline – Neuroinflammation

  1. Fatigue sensation following periphe
    ral viral infection is triggered by neuroinflammation: who will answer these questions?- 2016
  2. Minocycline plus N-acteylcysteine induces remyelination, synergistically protects oligodendrocytes and modifies neuroinflammation in a rat model of… – PubMed – NCBI – 2018
  3. Neuroinflammation of the spinal cord and nerve roots in chronic radicular pain patients – 2018


Minocycline – Neuropathic Pain

  1. Alternatives to Opioids in the Pharmacologic Management of Chronic Pain Syndromes: A Narrative Review of Randomized, Controlled, and Blinded Clinical Trials
  2. Effect of Minocycline on Lumbar Radicular Neuropathic Pain – 2015
  3. Experimental Drugs for Neuropathic Pain – 2018
  4. Enhancement of antinociception by coadministration of minocycline and a non-steroidal anti-inflammatory drug indomethacin in naïve mice. – 2010
  5. The effects of pregabalin and the glial attenuator minocycline on the response to intradermal capsaicin in patients with unilateral sciatica – 2012
  6. Minocycline and pentoxifylline attenuate allodynia and hyperalgesia and potentiate the effects of morphine in rat and mouse models of neuropathic p… – PubMed – NCBI
  7. Minocycline attenuates the development of diabetic neuropathic pain: possible anti-inflammatory and anti-oxidant mechanisms. – PubMed – NCBI – 2011
  8. Minocycline enhances the effectiveness of nociceptin:orphanin FQ during neuropathic pain – 2014
  9. Minocycline injection in the ventral posterolateral thalamus reverses microglial reactivity and thermal hyperalgesia secondary to sciatic neuropathy. – PubMed – NCBI – 2011
  10. Minocycline through attenuation of oxidative stress and inflammatory response reduces the neuropathic pain in a rat model of chronic constriction injury – 2018
  11. Paradoxical effect of minocycline on established neuropathic pain in rat. – 2017
  12. Targeting the Endocannabinoid System for Prevention or Treatment of Chemotherapy-Induced Neuropathic Pain – Studies in Animal Models – 2018
  13. Targeting the Microglial Signaling Pathways – New Insights in the Modulation of Neuropathic Pain. – 2016

Minocycline – Opioid Analgesic Tolerance

  1. A novel role of minocycline: attenuating morphine antinociceptive tolerance by inhibition of p38 MAPK in the activated spinal microglia. – PubMed – NCBI


Minocycline – Opioid-induced respiratory depression

  1. Glial TLR4 signaling does not contribute to opioid-induced depression of respiration – 2014
  2. Incidence, Reversal, and Prevention of Opioid-induced Respiratory Depression – 2009
  3. Microglia attenuate the opioid-induced depression of preBötzinger Complex (preBötC) inspiratory rhythm in vitro via a TLR4-independent pathway | The FASEB Journal
  4. Minocycline suppresses morphine-induced respiratory depression, suppresses morphine-induced reward, and enhances systemic morphine-induced analgesia – 2008


 Minocycline – Post-operative pain

  1. The efficacy of a glial inhibitor, minocycline, for preventi
    ng persistent pain after lumbar discectomy: a randomized, double-blind, controlled study. – PubMed – NCBI – 2013
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