Open Source Security Blogs

Wazuh & Keycloak using SAML

Use case:

Set up Keycloak for Authentication using SAML protocol in Wazuh.

Keycloak configuration:

  • Create a new client with the protocol set to saml :
  • Configure it to use the below options:
  • Add a role naming it Administrator:
  • Add a Role listmapper:
  • Navigate to Installation to generate the IDP and SP metadata files:
  • The idp.entity_id & exchange_keys are included in the idp-metadata.xml file:

Wazuh indexer configuration:

  • Place the content of idp-metadata.xml & sp-metadata.xml respectively within /etc/wazuh-indexer/certs/idp_metadata.xml & /etc/wazuh-indexer/certs/sp_metadata.xml setting the ownership to wazuh-indexer :
chown wazuh-indexer:wazuh-indexer /etc/wazuh-indexer/certs/sp_metadata.xml
chown wazuh-indexer:wazuh-indexer /etc/wazuh-indexer/certs/idp_metadata.xml
  • Configure the Wazuh indexer to use SAML by modifying /usr/share/wazuh-indexer/plugins/opensearch-security/securityconfig/config.yml : 
---
_meta:
  type: "config"
  config_version: 2

config:
  dynamic:
    http:
      anonymous_auth_enabled: false
    authc:
      internal_auth:
        order: 0
        description: "HTTP basic authentication using the internal user database"
        http_enabled: true
        transport_enabled: true
        http_authenticator:
          type: basic
          challenge: false
        authentication_backend:
          type: internal
      saml_auth:
        order: 1
        description: "SAML provider"
        http_enabled: true
        transport_enabled: false
        http_authenticator:
          type: saml
          challenge: true
          config:
            idp:
              metadata_file: /etc/wazuh-indexer/certs/idp_metadata.xml
              entity_id: http://192.168.0.92:8080/realms/master
            sp:
              entity_id: WazuhSAMLID
              metadata_file: /etc/wazuh-indexer/certs/sp_metadata.xml
            kibana_url: https://192.168.0.144/
            roles_key: Roles
            exchange_key: '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'
        authentication_backend:
          type: noop
  • Load the new security configuration:
export JAVA_HOME=/usr/share/wazuh-indexer/jdk &&  /usr/share/wazuh-indexer/plugins/opensearch-security/tools/securityadmin.sh -cd /usr/share/wazuh-indexer/plugins/opensearch-security/securityconfig/ -icl -key /etc/wazuh-indexer/certs/admin-key.pem -cert /etc/wazuh-indexer/certs/admin.pem -cacert /etc/wazuh-indexer/certs/root-ca.pem -h localhost -nhnv

Wazuh Dashboard configuration:

  • Set the authentication to saml by adding below to /etc/wazuh-dashboard/opensearch_dashboards.yml :
opensearch_security.auth.type: "saml"
server.xsrf.whitelist: ["/_opendistro/_security/saml/acs", "/_opendistro/_security/saml/acs/idpinitiated", "/_opendistro/_security/saml/logout"]

As this might be solved in future versions you should perform the next step only if you are facing logout issue (https://forum.opensearch.org/t/saml-issue-on-logout/5617/14).

  • Modify the logout endpoint in /usr/share/wazuh-dashboard/plugins/securityDashboards/server/auth/types/saml/routes.js by changing it from /auth/logout to /logout: 
    this.router.get({
      path: `/logout`,
      validate: false
    }, async (context, request, response) => {
      try {
        const authInfo = await this.securityClient.authinfo(request);
        this.sessionStorageFactory.asScoped(request).clear(); // TODO: need a default logout page

        const redirectUrl = authInfo.sso_logout_url || this.coreSetup.http.basePath.serverBasePath || '/';
        return response.redirected({
          headers: {
            location: redirectUrl
          }
        });
      } catch (error) {
        context.security_plugin.logger.error(`SAML logout failed: ${error}`);
        return response.badRequest();
      }
    });
  }

}

exports.SamlAuthRoutes = SamlAuthRoutes;
  • Restart Wazuh dashboard: systemctl restart wazuh-dashboard

DEMO:

I hope you find it useful 🙂

EL WALI KARKOUB

, , ,

105 responses to “Wazuh & Keycloak using SAML”

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  65. Li-hua Yao () must be contacted if someone desires to request the
    information from this examine. This part collects any knowledge citations, information availability statements,
    or supplementary materials included in this article.
    The data offered on this examine can be found in this article and the
    accompanying Supplementary Supplies. In summary, MIFs promote myoblast proliferation, myogenic differentiation, and muscle regeneration by upregulating muscle regulatory genes.
    On the other hand, they inhibit proliferation and adipogenic differentiation by downregulating adipogenic regulatory genes.

    In-depth evaluation of the bindings between MSTN and the activin kind IIB receptor (ACVRIIB) or
    FMOD confirmed that the residues at positions 22–31 of MSTN had been predominantly involved with both
    interactions. Computational alanine scanning of MSTN–FMOD and
    MSTN–ACVRIIB complexes showed that MSTN residues in this region were main contributors to ACVRIIB
    and FMOD binding (Supplementary Tables S1–S3).
    Last however not least, EP1LOGUE contains a proprietary vasodilating and nitric oxide-boosting formulation of gallate-enhanced oligomers derived from grape seeds and marketed as 10x more powerful than the
    basic citrulline. This means better blood move to the
    muscle tissue – and thus enhanced supply of epicatechin and
    urolithin B. In brief, if you want to develop muscle tissue, you have to control myostatin and enhance
    follistatin.
    In a section 2 medical trial of patients with myelodysplastic syndromes (MDS), ACE-011 successfully decreased transfusion burden in 47% of sufferers with a high transfusion burden, while elevating Hb levels in 58% of patients with a low transfusion burden [88].

    Likewise, in a part 2 clinical trial involving patients with Îē-thalassemia, 75% of
    non-transfusion-dependent patients treated with greater doses resulted in a sustained improve
    in Hb levels [89]. In addition, preclinical research in animal
    fashions of pulmonary arterial hypertension (PAH) confirmed consistent efficacy
    of sotatercept [90], and a phase 2 human trial for the remedy of
    PAH is at present ongoing. Current literature means that MSTN acts
    as a mediator between muscle and bone metabolism, influencing
    bone formation and reworking via paracrine and endocrine mechanisms
    [8].
    We additionally measured biochemical indicators, together with LG, MG,
    LA, CK, LDH, and BUN levels, to evaluate fatigue.
    Previous research has highlighted the importance of glycogen as an power
    source during exercise, with adequate hepatic glycogen and myoglycogen enhancing endurance and sustaining high-intensity
    exercise18,19,20. LA is a key indicator for assessing fatigue levels as it is the end product of
    anaerobic glycolysis throughout high-intensity train. This process can lead to a decrease in the muscle and
    blood pH, which can trigger tissue injury and elevated
    fatigue21,22. Elevated LDH and CK levels replicate skeletal muscle cell necrosis and tissue damage23,24.
    When fatigue arises from high-intensity train, inadequate vitality from carbohydrate and fats metabolism happens, resulting in protein and amino acid depletion and
    elevated urea nitrogen levels22.
    It wasn’t acquired by Wealthy Gorilla Restricted until 2019, and
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    stacking Epitech with different prime anabolic muscle-building supplements like Annihilate and Archidone, particularly if you’re serious about gaining muscle and
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    Epi-Triol by House of Muscle is an advanced muscle constructing complement that helps you construct hard, lean muscle and energy.

    SOD exercise was decided utilizing the WST-8 methodology and MDA activity was evaluated primarily based on the principle of MDA-TBA adduct
    formation. NAD acts as a hydrogen acceptor, and the conversion of lactate to pyruvate is catalyzed by lactate dehydrogenase.
    The ensuing pyruvate then reacted with dinitrophenylhydrazine to type dinitrophenylhydrazone.
    Absorbance readings have been recorded at 450, 440, and 553 nm using a spectrophotometer and
    microplate reader (Thermo Fisher, USA). C2C12 cells, 3T3-L1 cells, or mouse MSCs (1000 cells/mL) were cultured in development
    media supplemented with one thousand nM MIF peptides (MIF1,
    MIF2, Ac-MIF1, Ac-MIF2, MIF1-NH2, MIF2-NH2, Ac-MIF1-NH2, or Ac-MIF2-NH2) for 1 day.
    Media was then removed, and cells were washed with DMEM (C2C12
    and 3T3-L1 cells) or Ham’s F10 (Mouse MSCs) media and then incubated with zero.5 mg/mL of
    MTT reagent (Sigma-Aldrich, St. Louis, MO, USA) for 1 h at 37 °C.

    Indeed, myostatin is taken into account a extremely druggable goal and the present research demonstrates a possible
    novel dietary strategy for its modulation that negates prior problems
    with poor ET/EA bioavailability. Polyphenolic plant extracts have demonstrated anti-inflammatory and
    anti-catabolic results in vitro, however their significant translation into people
    stays elusive. Urolithin A (UA), a gut-derived metabolite of ellagitannins,
    has shown promise for bettering muscle function and metabolic health
    in rodent models. This research aimed to explore the impact of UA
    on insulin and anabolic sensitivity in human skeletal muscle cells.

    Elevated angiotensin ranges diminish the satellite tv for pc
    cell reservoir and impair muscle regeneration capability.
    Furthermore, CKD stimulates the renin-angiotensin mechanism, which
    triggers caspase three in muscle tissue and promotes actin cleavage, thus
    precipitating muscle atrophy. Angiotensin II enhances muscle proteolysis by stimulating the UPS and
    the TGF-Îē process, while concurrently reducing circulatory
    IGF-1 concentrations, a principal cause of muscle mass discount [96].

    In summary, CKD leads to elevated ranges of angiotensin II within the physique,
    contributing to skeletal muscle atrophy. After confirming the optimistic effects of Ac-MIF1 and Ac-MIF2-NH2 on myogenesis,
    we investigated the regenerative potentials of those peptides in CTX-injected mouse gastrocnemius muscle tissue.
    There had been no important differences in physique or gastrocnemius muscle weights
    between peptide-injected and non-injected muscles, which could be attributed to the
    reality that the peptide-injected mice experiments have been conducted after a
    short interval (7 days). MSCs are liable for the maintenance and recovery of SM following injury
    and specific nuclear Pax7, which regulates MYOD and MYF5 [32,33].

    Due to this limitation in examine design, the authors can not decide with certainty whether the increased myostatin concentration occurred during the immobilization part or the restoration phase,
    or each. This is especially relevant in light of a recent 10-day mattress rest study that discovered
    an unexpected improve in circulating myostatin after two days of restoration, however not in the course of the unloading interval (Oranger et al., 2022).
    Why did the authors resolve to not collect blood samples on day 14
    (onset of the immobilization phase) and day 28 (end of the
    immobilization phase)?
    In addition, ghrelin has been proven to forestall muscle
    atrophy in rats by enhancing AKT phosphorylation, suppressing the MSTN pathway, and activating
    myogenin and MyoD (Chen et al., 2015). Ghrelin formulations for parenteral
    administration are being developed (Garin et al., 2013).
    However, administration by injection over prolonged durations can end result in poor affected person compliance
    and therapy failure, and ghrelin is vulnerable to enzymatic breakdown in blood when delivered intravenously (Brimijoin et al., 2016).

    Ghrelin liposomes coated with chitosan are being developed for nose-to-brain administration for the therapy of cachexia (Salade et al., 2017).

    It also focuses on findings in myostatin biology which will have
    implications for the event of antimyostatin therapies. Customers are satisfied with
    the muscle strength and recovery advantages of the nutritional supplement.
    The product speeds up muscle recovery, making their exercises easier and allowing them to hold
    up muscle mass. Two traits of senescent MPCs probably lead to the frequent description of CKD
    as an inflammatory persistent condition. Initially, senescent cells exhibit resistance to apoptosis, resulting in their
    continued existence in the senescent part. Secondly, they
    formulate an SASP characterised by sustained cytokine technology [57].

    However, we’ve not stopped since, as we’ve seen impressive
    features in energy, muscle mass, and restoration. If you’re looking to achieve some extra
    muscle mass whereas concurrently growing energy and energy, then supplementing with Epicatechin could probably be
    for you. For occasion, a 12-week study discovered that whole eggs and egg
    whites lowered myostatin with no difference
    between the teams. (Bagheri et al., 2020) Furthermore, follistatin, which is an inhibitor
    of myostatin, was increased. This has been investigated and proven in each animal research
    and research with people (here’s one study example, and right
    here is another). Not solely have been they no stronger than their wild, much
    less huge counterparts, but when particular drive was
    measured (i.e. energy as a function of muscle size) they have been weaker.

    The hypertrophic pathway triggered by resistance training is certainly one of them, and a
    vital one when deciding whether or to not try taking a industrial or lab grade myostatin inhibitor
    (keep studying and I’ll get to that half soon).

    Inhibiting MSTN may have therapeutic purposes in selling bone regeneration and healing in bone fractures, osteoporosis,
    rheumatoid arthritis, and osteoarthritis. In mice, administration of recombinant MSTN propeptide improved fracture healing
    in a fibula osteotomy mannequin [150]. Moreover, remedy
    of younger mice with ActRIIB-Fc led to elevated bone mass [151].

    Formulas of dietary supplements typically outpace the science behind their components — epicatechin supplements are one
    other instance of that development. Although it could enhance nitric oxide
    manufacturing and mitochondrial biogenesis, it’s unclear
    if epicatechin confers significant muscle-building advantages.

    Inhibiting myostatin is an example of disinhibition — when a molecule that normally
    inhibits a pathway is inhibited by one other molecule, an opposite impact results.
    In this case, the expression of myogenic factors increases when myostatin is inhibited.
    When myostatin binds to its receptor, ActRIIB, it activates a cellular pathway
    known as Smad that blocks genes from transcribing myogenic components.

    Protein synthesis and degradation homeostasis are required for the upkeep
    of healthy muscle mass and for sensitivity to bodily activity,
    hormonal steadiness, injury, and nutritional standing [1].
    The IGF1-Akt-mTOR pathway is a optimistic regulator of protein synthesis
    and is counterbalanced by the myostatin—Smad2/3 pathway, which acts as a
    negative regulator [5]. Imbalance within the myostatin—Smad2/3
    pathway causes muscle atrophy, which, in the context
    of most cancers, is called most cancers cachexia [6]. Naturally, muscle
    loss happens from 35 years of age and ~30% loss happens between the ages of 50 and eighty
    [7]. SM loss is the main attribute of growing older and illnesses
    similar to obesity, diabetes, and cancer [8,9]. Interleukin-15 (IL-15) is highly
    expressed in SM and has anabolic effects on SM protein dynamics
    (Quinn et al., 2002). IL-15 mRNA expression is up-regulated throughout myoblast differentiation and its administration inhibits the white adipose tissue deposition in rodents (Quinn et al., 2005).

    Spending cash on supplements that do not work will not only value you
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    Wonderful outcomes from quite a few research
    studies created an enormous curiosity in epicatechin. It
    can indeed promote greater muscle gains, better blood flow and higher testosterone
    ranges. Its most notable testosterone-supporting ingredient is patent KSM-66 extract of Ashwagandha (Withania somnifera).
    This extract has been tested in quite a few studies to
    be an effective natural testosterone booster, stress reducer,
    and muscle and strength gainer. ​This supplement targets myostatin and
    accommodates additional herbs to extend anabolic results, particularly well suited for bodybuilding.

    The management group had a larger range and interquartile range in LOAD scores for all 3 time
    factors compared with the treatment group (Table 2).
    The resulting massive variance in the management group
    compared with the remedy group likely is the rationale for a statistical difference within groups but not between teams.
    Due To This Fact, this statistically important difference
    throughout the treatment group could not mirror a clinically related change.

    The failure of ACE-083 to meet scientific endpoints
    ultimately led Acceleron to discontinue its improvement and shift its
    focus of TGF-Îē focusing on therapeutics away from muscle-dystrophic illnesses.
    Myostatin; also identified as development differentiation issue 8 (GDF8) has been nicely reported to negatively regulate
    muscle progress and size (Carnac et al., 2007; Chen et al., 2021).
    The putative involvement of MSTN in muscle atrophy has been documented
    in several research, prompting interest in MSTN as a therapeutic target to counteract muscle loss in patients with a range of muscle-wasting conditions
    (Baczek et al., 2020; Sartori et al., 2021).
    For astronauts on board the International House Station (ISS), even high-volume resistance train doesn’t absolutely stop muscle atrophy and weakness2,four and might become infeasible if astronaut health had been compromised.
    Pharmaceutical therapies that promote or preserve muscle mass and strength, alone or
    in combination with train or dietary interventions, are
    essential to take care of astronaut fitness
    throughout long-duration spaceflight missions. An improved
    understanding of mechanisms that underlie spaceflight-induced muscle loss is thus needed.

    Fortetropin (Canine Muscle Method; Myos, Cedar Knolls, New Jersey, USA), a nonthermal-pasteurized,
    freeze-dried, fertilized egg yolk product, was proven to have an abundance of proangiogenic and host-defense
    proteins compared to unfertilized egg yolk (10).

    Fortetropin is believed to advertise muscle development via
    the reduction of serum myostatin through an undefined mechanism, but the measured impact on serum myostatin ranges has various in studies (11,12).

    Nevertheless, a research in older women and men demonstrated no change in serum myostatin over 21 d of Fortetropin administration, regardless
    of demonstrating an 18% improve within the fractional synthetic fee of
    muscle protein in comparability to a placebo (13).

    However, there are a quantity of potential downsides to myostatin inhibition in people looking for athletic enhancement.
    Creatine and follistatin dietary supplements have not been approved by the FDA for medical
    use. Regulations set manufacturing requirements for them but don’t assure
    that they’re secure or effective. Some
    scientists assume myostatin inhibition should be additional researched for probably preventing weight problems and diabetes [29, 26].
    This impact has largely been seen in animal research on follistatin, a pure
    hormone that inhibits myostatin [26, 27, 28].
    Thus, Epi is the first compound ever famous, to favorably modulate both regulators of muscle growth and counsel will increase in energy.
    From a biomedical perspective, myostatin inhibitors are a kind of drug
    that target myostatin, a protein concerned in regulating muscle growth and
    growth. Myostatin inhibitors work by blocking the exercise of
    myostatin, which may lead to elevated muscle mass and energy.
    These inhibitors have potential purposes in treating muscle-wasting
    circumstances, corresponding to muscular dystrophy, and can also be used to reinforce muscle progress in athletes and bodybuilders.

    By inhibiting myostatin, these drugs can promote muscle hypertrophy and probably improve
    muscle function.
    Presently, no analysis exists in CKD that elucidates the signaling
    networks inhibiting NF-ΚB stimulating NRF2.
    Nonetheless, it is posited that this effect is
    mediated by way of the controlling of the enzymes MAFbx (atrogin-1) and MuRF1 throughout the ubiquitin-proteasome system.
    These techniques are activated in response to oxidative stress and inflammation, thereby enhancing the
    functioning of mitochondria [182,183,184]. Consequently, addressing
    the NRF2 axis with strategically formulated nutraceuticals could
    symbolize a viable treatment technique. Quite A Few investigations have sought
    to elucidate the mechanisms of NRF2 stimulation by nutritional substances and to substantiate their
    protective effects in skeletal muscle [185]. In a previous examine, inhibition of MSTN by
    antibody found no change in fat mass in an animal mannequin [37].

    References:

    What Is Gear Steroids

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