“The endocannabinoid system (ECS), comprising cannabinoid receptors, endogenous lipid ligands, and enzymes that regulate their synthesis and degradation, has emerged as an important modulator of neuroendocrine regulation.
This review summarises current evidence on the role of endocannabinoid signalling in hypothalamic-pituitary neuroendocrine circuits, with particular focus on the hypothalamic-pituitary-adrenocortical, gonadal, thyroid, and somatotropic axes, as well as prolactin and posterior pituitary hormones regulation.
Available data indicate that endocannabinoid signalling predominantly influences neuroendocrine function by modulating synaptic transmission within hypothalamic circuits. Acting mainly as retrograde messengers at presynaptic CB1 receptors, endocannabinoids regulate excitatory and inhibitory inputs to neurosecretory neurons and thus shape endocrine output in a context-dependent manner.
Among the systems discussed, the hypothalamic-pituitary-adrenocortical axis is the best characterised, with relatively well-defined links between glucocorticoid feedback and rapid endocannabinoid-mediated suppression of synaptic input to corticotropin-releasing hormone neurons.
In other neuroendocrine systems, evidence supports a predominantly modulatory, often inhibitory, role for endocannabinoid signalling, although the underlying cellular processes remain less well-defined and are largely based on preclinical studies. Interactions with glucocorticoids, gonadal steroids and neuropeptidergic pathways further underscore the integrative nature of ECS signalling.
Overall, the ECS should be viewed not as a primary endocrine driver, but as a dynamic regulatory network that fine-tunes the translation of neural activity into hormonal responses.”
“Background: Paroxysmal Sympathetic Hyperactivity (PSH) is a well-recognized complication following severe traumatic brain injury (TBI), with an incidence of 5-33% in the acute phase, characterized by episodic autonomic and motor hyperactivity. Management is often challenging, and a subset of patients develop refractory PSH despite optimized first- and second-line therapies. Cannabidiol (CBD) possesses neuroregulatory and autonomic-modulating properties demonstrated in preclinical TBI studies and epilepsy trials including Epidiolex studies, but its role in PSH has not been previously described.
Case presentation: We report the case of a 44-year-old South Indian gentleman with severe TBI following a road traffic accident (GCS 5: E1V1M3) with CT brain showing bilateral frontotemporo-parietal acute subdural hematoma with mass effect. He underwent emergency bilateral decompressive craniectomy and required mechanical ventilation with tracheostomy. Three weeks post-injury, he developed recurrent PSH episodes (4-6 episodes per day) characterized by severe tachycardia (heart rate 140-180 bpm), hypertension (systolic blood pressure > 180 mmHg), hyperthermia (up to 40 °C), diaphoresis, and dystonic posturing. The diagnosis of PSH was established using the Paroxysmal Sympathetic Hyperactivity Assessment Measure (PSH-AM), with a total score of 28 (Clinical Feature Scale: 18, Diagnosis Likelihood Tool: 10), indicating probable PSH. Infective, metabolic, epileptic, and structural causes were excluded. Despite treatment with multiple conventional agents at maximum tolerated doses-including bromocriptine (titrated from 1.25 mg twice daily to 40 mg/day), baclofen (10 mg/day), gabapentin (titrated from 150 mg/day to 300 mg/day), propranolol (15 mg three times daily), clonidine (0.2 mg/day), dexmedetomidine infusion (72-h infusion), and fentanyl (infusion followed by patches)-the autonomic storms persisted, fulfilling criteria for refractory PSH.
Cannabidiol oil (100 mg/mL) was therefore initiated as adjunctive therapy at 100 mg twice daily (approximately 3 mg/kg/day) and titrated to a 100-150-100 mg/day regimen over one week via nasogastric tube. Within the first week, there was a marked reduction in episode frequency (from 4 to 6 per day to less than 1 per 48 h) and severity, with PSH-AM scores decreasing from 28 (CFS: 18, DLT: 10) to 16 (CFS: 6, DLT: 10), and opioid and sedative infusions were successfully withdrawn. By the second week, complete resolution of PSH episodes was achieved with a PSH-AM score of 4. No adverse effects were observed, including no hepatic dysfunction, excessive sedation, or hemodynamic instability.
Conclusions: This case highlights a potential adjunctive role for cannabidiol in refractory PSH following severe TBI. While causality cannot be inferred from a single observation, the sustained clinical improvement after failure of conventional therapies warrants further prospective investigation.”
“Lung cancer is the major cause of cancer-related mortality worldwide.
Many of these over-express epidermal growth factor receptor (EGFR), and are usually highly aggressive and resistant to chemotherapy.
Recent studies have shown that Δ-9 Tetrahydrocannabinol (THC), the major component of Cannabis sativa, possess anti-tumor properties against various types of cancers. However, not much is known about its effect on lung cancer.
In this study, we sought to characterize the effect of THC on EGF-induced growth and metastasis of human non small lung cancer cell (NSCLC) lines A549 and SW-1573.
We demonstrate that these cell lines and primary tumor samples derived from lung cancer patients express cannabinoids receptors CB1 and CB2, the known targets for THC action. We further show that THC inhibits EGF-induced growth in these cell lines. In addition THC attenuated EGF-stimulated chemotaxis and chemoinvasion.
Next we characterized the effect of THC on in vivo lung cancer growth and metastasis in a murine model.
A549 cells were implanted in SCID mice (n=6 per group) through subcutaneous and intravenous injections to generate subcutaneous and lung metastatic cancer, respectively. THC (5mg/kg body wt.) was administered once daily through intraperitoneal injections for 21 days. The mice were analyzed for tumor growth and lung metastasis.
A significant reduction (~50%) in tumor weight and volume were observed in THC treated animals compared to the vehicle treated animals. THC treated animals also showed a significant (~60%) reduction in macroscopic lesions on the lung surface in comparison to vehicle treated control.
Immunohistochemical analysis of the tumor samples from THC treated animals revealed anti-proliferative and anti-angiogenic effects of THC with significant reduction in staining for Ki67, a proliferative marker and CD31, an endothelial marker indicative of vascularization. Investigation into the signaling events associated with reduced EGF-induced functional effects revealed that THC also inhibits EGF-induced Akt phosphorylation. Akt is a central signaling molecule of EGFR-mediated signaling pathways and it regulates a diverse array of cellular functions, including proliferation, angiogenesis, invasion and apoptosis.
Cumulatively, these studies indicate that THC has anti-tumorigenic and anti-metastatic effects against lung cancer.
Novel therapies against EGFR overexpressing, aggressive and chemotherapy resistant lung cancers may include targeting the cannabinoids receptors.”
“Non-small cell lung cancer (NSCLC) remains a leading cause of cancer-related mortality worldwide, driven in part by persistent activation of pro-survival pathways such as STAT3 and NF-κB.”
“Cannabidiol (CBD), a non-psychoactive phytocannabinoid, has emerged as a potential anti-cancer agent; however, its mechanisms in NSCLC remain incompletely defined. In particular, CBD has not been systematically investigated for its ability to simultaneously suppress both constitutive and inducible STAT3/NF-κB activation, while coordinating apoptosis and autophagy in NSCLC. Furthermore, its role as a chemosensitizer in combination with paclitaxel remains to be validated in vivo.”
“Human NSCLC cell lines (A549, PC9, and H1299) were treated with cannabidiol (CBD), alone or in combination with paclitaxel. Apoptosis and autophagy were evaluated via caspase-3/7 activity, Western blotting, and immunocytochemistry. The effects of CBD on STAT3 and NF-κB signaling were assessed using EMSA, luciferase reporter assays, and nuclear translocation analysis. Anti-tumor efficacy was further validated in a xenograft mouse model.”
Results
“Here, we demonstrate that CBD reduced cell viability in NSCLC cells (A549 and PC9), while showing less cytotoxicity in normal lung fibroblasts. Mechanistically, CBD induced apoptosis and autophagy and suppressed STAT3 and NF-κB activation at the levels of phosphorylation, nuclear localization, and transcriptional activity. These effects were also observed in inducible signaling models using IL-6–stimulated H1299 cells. Importantly, CBD enhanced the efficacy of paclitaxel, a commonly used chemotherapeutic agent, by synergistically inducing apoptosis and autophagy and further suppressing STAT3/NF-κB signaling. In a xenograft mouse model, CBD treatment significantly reduced tumor growth without affecting body weight, and combination therapy with paclitaxel led to the most pronounced tumor suppression. Tumor tissue analyses confirmed that CBD downregulated phosphorylated STAT3 and p65, reduced proliferation marker Ki-67, and increased expression of cleaved PARP, LC3 II, and other cell death-associated proteins.”
Conclusion
“Our findings provide preclinical evidence that CBD exerts potent anti-tumor activity in NSCLC by coordinating inhibition of oncogenic signaling and activation of programmed cell death pathways. To our knowledge, this study provides evidence that CBD concurrently inhibits STAT3 and NF-κB signaling, affecting both constitutive and inducible activation in NSCLC, and enhances paclitaxel efficacy in vivo, thereby establishing a novel mechanistic and translational basis for its therapeutic potential.”
“These results support the therapeutic effect of CBD as a potential adjuvant in lung cancer treatment.”
“Cannabidiol (CBD), a non-psychoactive phytocannabinoid derived from Cannabis sativa, has gained attention for its broad pharmacological actions, including anti-inflammatory, anti-proliferative, and pro-apoptotic effects.”
“Of particular interest, CBD has been shown to exert potent anti-cancer activities across various tumor types by modulating multiple intracellular pathways.”
“Background/Objectives: Chronic low back pain (CLBP) affects approximately 20% of the global population and is a leading cause of years lived with disability. Long-term, real-world evidence for inhaled cannabis in patients refractory to conventional multimodal therapy remains scarce. We assessed the five-year efficacy and safety of inhaled cannabis in CLBP patients who had documented failure of ≥1 year of opioid analgesics, anticonvulsants, antidepressants, NSAIDs, and physiotherapy, with each patient serving as their own historical control.
Methods: We analyzed prospectively collected clinical data from 241 consecutive adults with treatment-refractory CLBP (mean age 49.3 ± 14.9 years; 37.8% female; mean pain duration 15.1 years) initiated on inhaled medical cannabis (predominantly smoking, THC 4-22%, CBD 2-22%) in a single-center tertiary orthopedic clinic between 2020 and 2025 (Hasharon Hospital, Rabin Medical Center, Israel; IRB protocols 0807-21-RMC and 0634-25-RMC). Year-0 outcomes during conventional therapy were compared with outcomes at Years 1-5 on cannabis. Primary outcomes were the Numeric Rating Scale (NRS), Oswestry Disability Index (ODI), and Brief Pain Inventory severity/interference (BPI-S/BPI-I). Concomitant-medication trajectories were a secondary outcome. The primary analysis was a mixed model for repeated measures (MMRM) with random intercept and slope, REML estimation, and time as a categorical fixed effect. Multiple imputation (MAR, m = 20, Rubin’s rules) was the primary missing-data approach; complete-case and tipping-point pattern-mixture sensitivity analyses were used. A multivariate Hotelling T2 provided a joint test across the four correlated PROMs. Concomitant-medication discontinuation was modeled with GEE logistic regression and exact McNemar tests. Time to discontinuation was estimated by Kaplan-Meier and Cox regression. The Bonferroni-adjusted significance threshold for the four primary outcomes was α = 0.0125. BioWell gas-discharge-visualization (GDV) parameters were exploratory only.
Results: Of 241 patients, 238 (98.8%) provided Year-5 data and 224 (92.9%) remained on cannabis at Year 5; only five patients (2.1%) discontinued for adverse events or inefficacy. All four primary PROMs improved markedly and durably. MMRM-estimated Year-5 minus Year-0 changes were: NRS -5.36 (95% CI -5.65, -5.07), ODI -17.68 (95% CI -19.73, -15.63), BPI-S -6.73 (95% CI -6.99, -6.47), and BPI-I -3.41 (95% CI -3.65, -3.16); all four contrasts had |z| ≥ 16.9 and p < 10-20. MI-pooled estimates were within 0.05 of MMRM (FMI < 0.03 for all outcomes). Hotelling T2 was F(4, 232) = 872.8, p < 10-20. At Year 5, 89.2% achieved ≥30% NRS reduction, 77.2% ≥ 50%, and 93.4% met the NRS minimum clinically important difference (MCID); ODI MCID 65.6%, BPI-S MCID (≥1 pt) 98.3%, BPI-I MCID (≥1 pt) 91.3%. Concomitant opioid use fell from 100% at baseline to 4.6% at Year 5 (within-patient absolute risk reduction 95.4%, McNemar exact p = 1.16 × 10-69), NSAID from 100% to 7.1%, SSRI/SNRI from 80.5% to 5.4%, and gabapentinoid from 38.6% to 2.5%. The ARR-derived NNT for opioid discontinuation was 1.05; this NNT is referenced to each patient’s own documented maximal-conventional-therapy state and is not equivalent to a between-arm randomized-trial NNT. Cannabis dose × time interaction was consistent with no pharmacological tolerance (β = -0.0044 per gram-month per year, p = 0.074). Across 1205 patient-years of cannabis exposure (calculated as 241 patients × 5 follow-up years from Year 1 through Year 5; baseline Year 0 represents pre-cannabis state and is not included in person-time on cannabis), 1338 organ-system AE events were recorded at 1.110/patient-year (Poisson 95% CI 1.05-1.17); 99.8% of graded events were mild (grade 1), with ocular (476 events, 0.40/PY), cognitive (460, 0.38/PY), and gastrointestinal (368, 0.31/PY) reactions predominating. The Year-3 retention dip reflected a documented telemedicine-clinic phenomenon during 2022-2024, with patients returning to in-person follow-up by Year 4-5. BioWell GDV discriminated NRS ≥ 4 only at chance level (BWS AUC 0.574, 95% CI 0.54-0.60; BWV AUC 0.51).
Conclusions: In a treatment-refractory CLBP cohort with five-year longitudinal follow-up, inhaled cannabis was associated with large, sustained, and statistically robust improvements in pain, disability, and pain interference, accompanied by near-total displacement of opioids, NSAIDs, antidepressants, and gabapentinoids. These observational associations, although mechanically less susceptible to bias for the binary medication-discontinuation outcomes than for self-reported PROMs, cannot be interpreted causally in the absence of a concurrent randomized control arm and may reflect a combination of pharmacological effect, regression to the mean from a high pre-treatment baseline, expectancy and self-selection effects intrinsic to an actively chosen open-label therapy, and secular trends in pain reporting. The within-patient benefit-risk profile-ARR-derived NNT ≈ 1 for opioid sparing against a predominantly mild adverse-event burden-supports consideration of cannabis as a potentially clinically meaningful, opioid-sparing option in patients who have failed multimodal conventional therapy, pending confirmation in randomized comparative trials.”
“Inhaled medical cannabis has emerged as a candidate analgesic for refractory chronic-pain syndromes.
Mechanistically, exogenous Δ9-tetrahydrocannabinol (THC) and cannabidiol (CBD) modulate the endocannabinoid system through CB1- and CB2-receptor signaling, with downstream effects on descending pain modulation, peripheral nociceptor sensitization, and affective dimensions of suffering.”
“These data support consideration of inhaled cannabis as a potentially clinically meaningful, opioid-sparing option for patients who have failed conventional multimodal therapy.”
“Ultraviolet A (UVA) radiation disrupts the redox balance of melanocytes and may lead to the development of melanoma, highlighting the need for new skin protection strategies.
This study assessed the effect of phytocannabinoids [cannabigerol (CBG), cannabidiol (CBD), and CBG + CBD] on redox homeostasis in control and UVA-exposed melanocytes and in melanoma cells (SK-Mel-5).
UVA radiation increased the activity of prooxidant enzymes in both melanocytes and SK-Mel-5 cells and, consequently, the level of reactive oxygen species (ROS) (approx. 2-fold). It also activated nuclear factor erythroid 2 (Nrf2), as reflected by increased expression of heme oxygenase 1 (HO-1) (melanocytes approx. 2-fold; SK-Mel-5 approx. 7-fold). Concomitantly, antioxidant mechanisms were impaired, as demonstrated by reduced superoxide dismutase (SOD1/SOD2) activity and impaired glutathione and thioredoxin function. These changes were accompanied by increased levels of oxidative damage markers (isoprostanes, 4-hydroxynonenal-4-HNE, and 4-HNE-protein adducts) (43-100%) and increased inflammatory signaling, including increased expression of nuclear factor kappa B (NF-κB) subunits (melanocytes: p52 ~2-fold, p65 ~75%; SK-Mel-5: ~4-4.5-fold) and tumor necrosis factor alpha (TNF-α; ~30%).
Phytocannabinoid treatment modulated these UVA-induced changes.
In SK-Mel-5 cells, phytocannabinoids normalized the activity of prooxidant enzymes and consequently reduced ROS levels (~30%). They also reduced Nrf2 activation and HO-1 expression; however, CBG increased HO-1 level in melanocytes (~25-40%). Furthermore, phytocannabinoids enhanced antioxidant defense by increasing SOD activity, particularly in melanocytes (~10-40%), and restoring the glutathione and thioredoxin systems. Markers of oxidative damage were reduced by approximately 23-37% after treatment. Furthermore, phytocannabinoids attenuated NF-κB activation (p52 ~18-28%, p65 ~25-29% in melanocytes; ~20% in SK-Mel-5), while TNF-α levels remained unchanged. The effects in non-irradiated cells were modest (<15%).
These results suggest that phytocannabinoid-mediated modulation of redox balance may stabilize melanocytes exposed to UVA radiation and potentially reduce the risk of neoplastic transformation. However, the observed protective effects in SK-Mel-5 cells require further investigation and detailed molecular analysis.”
“The observed stabilizing effect of phytocannabinoids on the redox homeostasis of UVA-irradiated melanocytes is particularly relevant, as it may reduce conditions that favor neoplastic transformation.”
“Cannabinoids are potential anticancer agents for the add-on treatment of malignant tumors.
Here, the effects of the previously less-explored non-psychoactive phytocannabinoids cannabigerol (CBG) and cannabichromene (CBC) on survival, apoptosis, and mitochondrial function were assessed in A549 and H460 lung cancer cells.
CBG and CBC triggered concentration-dependent cell death, autophagy, and mitochondrial apoptosis in both cell lines, with apoptosis indicated by Annexin V staining, activation of caspase-8, -9, and -3/7, loss of mitochondrial membrane potential, and elevated cytosolic levels of mitochondrial cytochrome c. CBG also upregulated ATF4, a stress-responsive transcription factor involved in autophagy and apoptotic signaling, and enhanced PARP cleavage. Both cannabinoids increased mitochondrial superoxide formation and reduced the mitochondrial oxygen consumption rate, with CBG additionally decreasing NDUFB8, a subunit of respiratory chain complex I.
Pharmacological receptor modulation showed that CBG- and CBC-induced cell death occurred independently of CB1, CB2, TRPV1, TRPM8, and PPARγ, whereas CBG-mediated cell death relied on PPARα, which also contributed to its apoptotic effects.
In summary, CBG and CBC induce apoptosis and cell death in A549 and H460 cells, with PPARα mediating the effects of CBG, highlighting its potential as a therapeutic target.”
“There is now substantial preclinical evidence supporting an anticancer action of various cannabinoids in different tumor entities.”
“This study investigates the effects of CBG and CBC on lung cancer cell survival, apoptosis, and mitochondrial function and bioenergetics, with particular emphasis on the role of PPARα in this process.
Here, we show convincing cytotoxic, pro-apoptotic and mitochondrial toxic effects of both cannabinoids.
More importantly, this study demonstrates for the first time a mediating role of PPARα in the induction of tumor cell death and apoptosis by CBG, which makes this non-psychoactive phytocannabinoid an interesting compound in the search for new targeted therapies for the treatment of malignant tumors.”
“The non-psychoactive phytocannabinoids CBG and CBC, which remain comparatively underexplored, were shown to induce pronounced pro-apoptotic effects and mitochondrial dysfunction in the human lung cancer cell lines A549 and H460, with CBG acting via the transcription factor PPARα to promote apoptotic cell death.”
“Industrial hemp (Cannabis sativa L.) has emerged as a sustainable source of bioactive compounds, with increasing interest in cosmeceutical applications for acne management.
This systematic review synthesises evidence on cannabinoid-containing hemp extracts, particularly cannabidiol (CBD), with emphasis on anti-inflammatory and sebostatic mechanisms, alongside formulation considerations and supply-chain sustainability.
Reporting followed PRISMA 2020 guidelines and encompassed preclinical and clinical evidence relevant to acne-associated outcomes. The review protocol was registered prospectively with PROSPERO (CRD420251272093).
Across cell-based, ex vivo and early clinical studies, CBD modulated key inflammatory mediators, including TNF-α, IL-1β, IL-6 and IL-8; normalised sebocyte activity and attenuated Cutibacterium acnes (Propionibacterium acnes)-induced inflammatory signalling.
Preliminary clinical observations indicate reductions in lesion counts and erythema, with generally favourable short-term tolerability; however, interpretation is limited by small sample sizes, predominantly non-randomised designs, heterogeneous formulations and frequent co-formulation with additional active ingredients. Evidence supporting direct antimicrobial efficacy and durable clinical benefit remains limited.
Lipid-rich hemp seed-derived products were considered only in a contextual capacity for barrier-supportive and nutritional properties and were excluded from efficacy synthesis unless cannabinoid content was verified. Sustainability analyses highlight hemp’s low water requirements, carbon sequestration potential and relevance to Sustainable Development Goal 3 (SDG 3: Good Health and Well-Being) and Sustainable Development Goal 12 (SDG 12: Responsible Consumption and Production), supporting its role in environmentally responsible cosmeceutical development.
Overall, CBD-containing hemp extracts show biologically plausible and clinically promising adjunctive potential for mild-to-moderate inflammatory acne, but current evidence remains preliminary. This review highlights the need for methodologically rigorous and transparent clinical studies, standardised formulations, validated outcome measures and the integration of sustainability metrics to strengthen evidence synthesis, clarify clinical relevance and guide responsible cosmeceutical development.”
“This systematic review focuses on CBD-containing hemp extracts and isolated CBD as cosmeceutical interventions for acne, explicitly distinguishing these from hemp seed oil, which is a cold-pressed nutritional oil with negligible cannabinoids.”
“Mechanistic evidence demonstrates that CBD exerts sebostatic and anti-inflammatory effects in human sebocytes and modulates keratinocyte responses to Cutibacterium acnes vesicles, providing biologically plausible pathways for clinical benefit.”
“Collectively, the available evidence supports the biological plausibility and emerging clinical relevance of CBD-containing hemp extracts in acne management”
“The anesthetic management of female dogs with mammary neoplasia, usually classified as ASA II and undergoing invasive procedures such as mastectomy and ovariohysterectomy, requires effective sedation and anesthetic stability due to the increased anesthetic risk associated with advanced age and underlying disease.
In this context, this study aimed to evaluate the sedative effects and reduction in anesthetic requirements of a full-spectrum cannabis oil (FSCO) containing cannabidiol (CBD) and tetrahydrocannabinol (THC) in female dogs undergoing mastectomy and ovariohysterectomy.
Twenty dogs were randomly assigned to two groups: group A (n = 10), treated with FSCO (0.02 mL/kg PO; 0.2 mg/kg CBD and 0.12 mg/kg THC) twice daily for seven days, plus 0.2 mL/kg (2 mg/kg CBD; 1.2 mg/kg THC) one hour before premedication; and group B (n = 10), treated with placebo. Groups A and B had similar ages (9.6; 10.2 years) and weights (7.4; 6.8 kg). Anesthesia was induced with propofol and maintained with sevoflurane. Outcomes included sedation scores, anesthetic requirements, rescue analgesia, responses to instrumentation, and adverse effects. The treated group required less propofol (2.33 vs. 5.98 mg/kg; p = 0.001) and lower sevoflurane concentrations from T0 to T4 (p < 0.05). Sedation scores were higher at 40 and 60 min (median of 4 vs. 0, and 6.5 vs. 0.5; p = 0.015 and p = 0.002, respectively). Fewer treated dogs required rescue analgesia (3/10 vs. 6/10; p = 0.178). No differences were observed in catheterization, intubation, or adverse effects.
Preoperative CBD/THC oil produced sedative effects and reduced anesthetic requirements without clinical complications.
These findings support the potential of cannabinoids as safe adjuvants in multimodal anesthesia in veterinary medicine.”
“The findings of this study indicate that preoperative administration of full-spectrum Cannabis sativa oil containing CBD and THC exerts significant sedative and anesthetic-sparing effects in female dogs with mammary neoplasia undergoing mastectomy and ovariohysterectomy.
The use of this phytocannabinoid extract significantly reduced the required doses of both propofol for induction and sevoflurane for maintenance, supporting its potential as an adjuvant in multimodal anesthetic protocols. Furthermore, the therapy was not associated with clinical adverse effects or compromised anesthetic safety, suggesting a favorable safety profile for perioperative use in oncological patients.”
“Bacterial infections can lead to wound inflammation and delay wound healing due to the cytotoxicity of the chemicals used in conventional wound dressings. Therefore, developing a new natural and non-toxic form of antibacterial hydrogel dressing is very important.
In this study, natural hemp fibers were used as the internal skeleton of hydrogels, combined with N-halamine antimicrobial nanosystems, and chitosan reaction was used to prepare Schiff base-type N-halamine hemp fiber-based hydrogels (N-hemp-gel).
This is mainly due to the unique polygonal cavity structure and phenolics of the hemp fibre itself, as well as the release of oxidized halide ions by N-halamine through electrostatic action, and the oxidation of bacterial enzymes and other intracellular compounds, which synergistically and significantly enhance the antimicrobial properties of the wound dressing.
Antimicrobial experiments showed that N-hemp-gel had significant bactericidal effects against both Escherichia coli (E. coli) and Staphylococcus aureus (S. aureus). In a mouse model of infected wounds, N-hemp-gel showed a 100 % wound healing rate on day 7 with no visible scarring. Storage stability confirmed that the chlorine content of N-hemp-gel decreased by only 25.5 % after 30 days at room temperature. Renewability demonstrated that the chlorine content of N-hemp-gel decreased by only 0.54 % after ten cycles.
This natural hemp fibre hydrogel with excellent antimicrobial properties, good storage stability and renewability, and green environmental protection has a broad prospect in the field of wound dressing and biomedicine.”
“Hemp fibre belongs to the bast natural fibre, is extracted from the stem of the hemp plant, is the highest toughness of natural fibres, can be naturally decomposed green fibre, through photosynthesis can be renewable, and more than 60 kinds of unique phenolic substances in the hemp hemp fibre makes hemp fibre has excellent anti-bacterial and anti-inflammatory function.”
“In this study, N-halamine Schiff base type cannabinoid cellulose based hydrogels were successfully prepared.
Antibacterial assays demonstrated that the material exhibits significant antibacterial activity against E. coli and S. aureus, effectively addressing the innate lack of antibacterial properties in cellulose materials, while also offering good storage stability and renewability.”
