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| 2.01 | The title is: Therapeutic Potential of Borneol: Mechanisms and Efficacy in Pain, Inflammation, Ischemic Stroke, Diabetes, Glioma, Cancer, Hypertension, Asthma, and Epilepsy |
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Title: Therapeutic Potential of Borneol: Mechanisms and Efficacy in Pain, Inflammation, Ischemic Stroke, Diabetes, Glioma, Cancer, Hypertension, Asthma, and Epilepsy
Neuroprotective Mechanisms of Borneol in Ischemic Stroke and Glioma Therapy
Borneol exerts neuroprotective effects in ischemic stroke through multiple mechanisms, including blood-brain barrier (BBB) modulation, anti-inflammatory actions, oxidative stress reduction, and anti-apoptotic pathways. It has been used in traditional Chinese medicine combinations for stroke treatment [1], with preclinical studies confirming its ability to improve BBB permeability for enhanced brain drug delivery [1][2]. Mechanistically, borneol targets tight junction (TJ) proteins: it translocates them from the cell membrane to the cytoplasm to reversibly open TJs for drug transport [2], and upregulates TJ proteins (claudin-5, occludin) to restore BBB integrity post-ischemia [3][4]. Additional neuroprotective mechanisms include reducing glutamate levels, activating GABAA receptors to block neuronal necrosis/apoptosis, increasing antioxidant enzyme activity via the Nrf2-ARE pathway, and regulating Ca²⁺ homeostasis [5]. Borneol also synergizes with other agents, as summarized below.
Borneol’s Therapeutic Effects in Ischemic Stroke and Glioma Models
| Application Context | Intervention | Key Outcomes | Citations |
|---|---|---|---|
| Ischemic stroke (MCAO model) | Borneol-based polymer NPs (6.4 mg·kg⁻¹ polymer) | Reduced infarct volume (7.6 ± 0.7%); 36.3% Longa score reduction; 30.1% decline in GFAP-positive cells; inhibited M1 microglia polarization; attenuated oxidative stress; decreased apoptotic cells | [2] |
| Ischemic stroke (meta-analysis, 15 animal studies) | Borneol | Reduced Evans blue content (WMD -4.16, 95% CI -4.68~-3.64); reduced brain water content (WMD -0.92, 95% CI -1.10~-0.75); improved neurological function scores (MD -0.42, 95% CI -0.65~-0.20) | [6] |
| Ischemic stroke (synergy) | Borneol + ligusticum chuanxiong Hort (LCH) | Enhanced BBB function (reduced Evans blue content); protected neurons | [4] |
| Ischemic stroke (synergy) | Borneol + mesenchymal stem cells (MSCs) | Improved neurological scores; reduced infarct volume; increased NeuN⁺ mature neurons | [7] |
| Ischemic stroke (synergy, MCAO model) | Borneol + tetramethylpyrazine (TMP) | Suppressed IL-1β expression; reduced infarct volume (26.79 ± 3.13% vs. 40.53 ± 5.59% in MCAO group); improved neurological outcomes | [8] |
| Glioma therapy | Borneol alone | Enhanced BBB/blood-brain cerebrospinal fluid barrier drug delivery (methotrexate, cisplatin); promoted immune cell migration; activated anti-tumor immunity; generated ROS to destroy tumor cells | [3] |
| Glioma therapy (synergy, in vitro) | Borneol + temozolomide (TMZ) | Inhibited C6/U251 cell proliferation/colony formation; increased autophagy (Beclin-1, LC3 II/I); degraded HIF-1α via mTORC1/eIF4E; increased apoptosis vs. TMZ alone | [9] |
| Glioma therapy (synergy, in vivo) | Borneol + TMZ | Reduced tumor weight; increased autophagosomes; elevated apoptotic cell numbers | [9] |
| Glioma therapy (synergy) | Borneol + 15Gy irradiation | Decreased tumor volume; downregulated HIF-1α/mTORC1/eIF4E; upregulated autophagy markers (LC3, Beclin-1) | [10] |
| Glioma therapy (formulation) | Borneol-modified paclitaxel liprosomes (BP-liprosome) | 85.71% tumor inhibition rate (vs. 49.00% for PTX solution); extensive tumor necrosis; low systemic toxicity | [11] |
In glioma therapy, borneol enhances drug delivery across the BBB and blood-brain cerebrospinal fluid barrier, increasing brain distribution of methotrexate and cisplatin while protecting the BBB [3]. It also potentiates immunotherapy by promoting immune cell migration across the BBB and activating anti-tumor immune responses [3]. Borneol alone or in combination generates reactive oxygen species (ROS) to destroy tumor cells [3], with synergistic effects alongside standard treatments like temozolomide (TMZ) and radiotherapy further inhibiting glioma progression through autophagy induction, HIF-1α degradation, and apoptosis promotion [9][10]. Additionally, borneol-modified paclitaxel liprosomes exhibit superior anti-tumor efficacy in glioma xenografts with minimal systemic toxicity [11].
Borneol-Mediated Barrier Modulation and Drug Delivery Enhancement
Borneol exhibits potent barrier modulation and drug delivery enhancement across multiple biological barriers, with well-characterized mechanisms and efficacy in preclinical models. Its effects are often concentration-dependent and vary by barrier type, with additional benefits from nanocarrier modification and combination formulations. Below is a consolidated summary of borneol’s efficacy, mechanisms, and associated drug delivery outcomes across key biological barriers:
Borneol-Mediated Drug Delivery Enhancement Across Biological Barriers
| Biological Barrier | Target Drug/Agent | Key Outcomes & Mechanisms | Citations |
|---|---|---|---|
| Skin (stratum corneum) | Osthole | Low concentrations (0.09%~0.54%): inhibits permeation; ≥0.54%: enhances cumulative permeation (Qn), permeation rate (PR), enhancement ratio (ER); 0.54% disrupts SC lipid regularity; 1.02% causes complete lipid disorder/separation (water pore formation) | [12] |
| Nasal | Geniposide (Ge) | Gardenia-Borneol co-compound formulations enable prompt/thorough nasal-to-brain Ge transport (comparable to i.v. administration; superior to gastrointestinal absorption) | [13] |
| Blood-brain barrier (BBB) | Antineoplastics, antibiotics, herbal drugs | 45/58 in vivo studies show significant CNS drug delivery improvement; reduces claudin-5/occludin expression, induces TJ protein translocation (membrane → cytoplasm); reduces MCAO-induced MMP-9 expression, increases TJ proteins (improves neurological function); increases hypothalamic 5-HT content (enhances ginkgolide brain uptake: 30% higher Cmax, 99% higher AUC₀→∞ vs. unmodified liposomes) | [14], [3], [15] |
| BBB (lipid bilayer simulations) | — | ≤16.42%: lateral expansion/decreased DPPC bilayer thickness (increased fluidity); ≥21.89%: non-bilayer structures (inverted micelles, irreversible changes); 7.64%: temporary water pore formation | [16] |
| Blood-brain tumor barrier (BTB) | Methotrexate, cisplatin | Enhances drug penetration into brain tissue; promotes immune cell migration across BBB (activates anti-tumor responses in glioma models) | [3] |
| Nanocarrier-modified BBB | Polymer NPs (p(PB)₁₀/(TB)₃₀) | Rapid localization in damaged MCAO mouse brain tissue; prolongs retention; reduces infarct volume by 7.6 ± 0.7% at 6.4 mg·kg⁻¹ dose | [2] |
| Multidrug resistance (MDR) | Geniposide | Inhibits P-glycoprotein (P-gp); increases geniposide flux in MDCK-MDR1 cells (concentration-dependent) | [15], [17] |
| Organ distribution | Tetramethylpyrazine (TMP) | Co-administration increases TMP Cmax in brain and heart vs. TMP alone | [8] |
| Selective permeation | Bicyclic monoterpenes (eucalyptol, camphor) | Enhances their barrier permeation; suppresses toxic thujone release | [18] |
| BBB safety | — | Reversible opening (returns to baseline 8 hours post-intragastric administration); no significant co-administration toxicity | [15] |
Borneol’s mechanisms of action include lipid layer disruption, tight junction modulation, water pore formation, and P-glycoprotein inhibition, with effects often tailored by concentration to avoid irreversible tissue damage. Modified nanocarriers further optimize targeted delivery to damaged brain regions, while combination formulations (e.g., Gardenia-Borneol co-compounds) address limitations like poor gastrointestinal absorption. Notably, its BBB-modulating effects are reversible and well-tolerated, supporting broad applicability in CNS disorders and cancer therapy.
Antihypertensive, Antidiabetic, and Antinociceptive Efficacy of Borneol
Borneol exhibits a range of therapeutic properties relevant to metabolic and nociceptive disorders, including antiglycemic, antihyperlipidemic, antioxidative, and antinociceptive effects [19][20]. Its antihypertensive potential is supported by in vitro studies showing concentration-dependent, endothelium-independent relaxation of aortic rings pre-contracted with phenylephrine or KCl⁻, with this vasorelaxation attenuated by K⁺ channel blockers and linked to interference with intracellular calcium mobilization [21]. In vivo, borneol demonstrates efficacy in reducing hypertension in L-NAME-induced and 2-kidney 1-clip (2K1C) renovascular hypertension rat models, with effects spanning biomolecular normalization, blood pressure reduction, and oxidative stress mitigation [22][23]. Mechanistically, borneol induces endothelium-independent vasorelaxation in mesenteric artery rings and inhibits calcium influx [23], while the genus Artemisia—containing borneol as a bioactive component—further supports its blood pressure regulatory role [24].
In diabetes, borneol acts by inhibiting Grb10 expression [25], with preclinical studies showing dose-dependent improvements in fasting blood glucose (FBG) levels, plasma insulin, β-cell function (HOMA-B), body weight, liver glycogen, glycated hemoglobin (HbA1c), and lipid profiles [26]. It also reverses diabetes-induced elevations in urea, alanine transaminase (ALT), and aspartate transaminase (AST) [26][25], enhances hepatic and renal antioxidant capacity (via increased superoxide dismutase [SOD], catalase [CAT], and reduced glutathione [GSH], plus decreased malondialdehyde [MDA]) [26][25], and improves pancreatic islet architecture and β-cell counts [26].
For antinociception, borneol exerts topical analgesic effects in humans via TRPM8 targeting [27]. In mice, borneol-containing preparations reduce acetic acid-induced writhing (via downregulated prostaglandin E2 [PGE2] and TRPM8) [28], attenuate both phases of formalin-induced nociception (with opioid receptor involvement) [29], and modulate TRP channels to support pain relief [30][31].
Borneol’s Therapeutic Effects Across Preclinical and Clinical Models
| Disorder Category | Model/System | Key Effects | Doses/Concentrations | Citations |
|---|---|---|---|---|
| Hypertension | In vitro aortic rings | Concentration-dependent, endothelium-independent relaxation (attenuated by K⁺ channel blockers) | Not specified | [21] |
| Hypertension | L-NAME-induced rats | Normalized liver amide A protein wavenumbers (3301 → 3420 cm⁻¹) and triglyceride C=O stretching shifts (1731 → 1747 cm⁻¹) | 50 mg/kg BW/day (borneol + 50 mg/kg BW/day L-NAME) | [22] |
| Hypertension | 2K1C renovascular rats | Lowered MAP (169 ± 9 → 123 ± 6 mmHg), SAP (196 ± 11 → 144 ± 5 mmHg), DAP (155 ± 4 → 103 ± 4 bpm); reduced sympathetic hyperactivity and MDA (22.8 ± 1.35 → 15.5 ± 1.51 nmol/mL); restored baroreflex sensitivity | 125 mg/kg/day (oral) | [23] |
| Diabetes | Diabetic rats | Reduced FBG (near control values); improved insulin, HOMA-B, body weight, liver glycogen, HbA1c, lipid profiles; reversed urea, ALT, AST elevations; enhanced antioxidant capacity; improved pancreatic islet architecture | 25 mg/kg and 50 mg/kg bw/day | [25][26] |
| Antinociception | Human topical application | Analgesic action (main target: TRPM8) | Not specified | [27] |
| Antinociception | Mice (acetic acid writhing) | Dose-dependent reduction (no motor function effects; downregulated PGE2 and TRPM8) | Topical borneol-containing essential oil (6 consecutive days) | [28] |
| Antinociception | Mice (formalin-induced) | Attenuated first phase (316 mg/kg) and dose-dependent second phase (ED50: 25.9 mg/kg) nociception; reversed by naloxone | 316 mg/kg (highest dose) | [29] |
Anticonvulsant, Anti-Inflammatory, and Anticancer Activities of Borneol
Borneol, a medicinal substance in Chinese and Indian traditional medicine, exhibits diverse therapeutic activities relevant to pain, inflammation, epilepsy, and cancer [27][20]. Its anti-inflammatory and analgesic properties have been documented in traditional medical applications, with records of borneol being prescribed to royal families and included in medicines for various symptomatic relief [30]. Mechanistically, borneol reduces pro-inflammatory cytokine secretion, lowering TNF-α, IL-1β, and IL-6 levels in serum, tissues, and LPS/ox-LDL-stimulated THP-1 macrophages [32][33]. For analgesia, it exerts topical efficacy in humans by targeting the transient receptor potential cation channel subfamily M member 8 (TRPM8) [27][34].
In epilepsy, borneol shows anticonvulsant activity in mouse models, with synergistic effects when combined with conventional antiseizure drugs (ASDs). In cancer, it augments the efficacy of anticancer agents and contributes to cytotoxic activity in combination with other compounds. The specific therapeutic effects and associated parameters of borneol across inflammation, epilepsy, and cancer are summarized below:
Borneol’s Therapeutic Effects and Key Parameters Across Disease Contexts
| Disease Context | Intervention/Model | Key Findings | Citations |
|---|---|---|---|
| Inflammation | Borneol-containing essential oil (BEO) nano-emulsions | Dose-dependent anti-inflammatory effects: IC₅₀ 5.3 mg/mL (heat-induced hemolysis), 0.26 mg/mL (hypotonic solution-induced hemolysis); 70.2% reduction in mouse ear swelling (prevention model) | [32] |
| Epilepsy | Mouse maximal electroshock (MES) model | Dose- and time-dependent anticonvulsant activity (ED₅₀: 255.4–448.1 mg/kg); potentiates PB/VPA (32%/35% ED₅₀ reduction); enhances brain concentrations of PB/VPA | [35] |
| Epilepsy | Borneol (300 mg/kg, i.p.) in MES model | 75% protection against seizures at 15 minutes post-administration | [36] |
| Cancer | Paclitaxel (PTX)-loaded liprosomes (BP-liprosomes) in C6 glioma xenografts | 85.71% tumor inhibition rate (vs. 49.00% PTX solution, 62.39% P-liprosomes); induces tumor necrosis without systemic toxicity | [11] |
| Cancer | Sage essential oils (borneol as component) | Among compounds associated with cytotoxicity against cancer cell lines; role linked to structural complexity in combination with other components | [37] |
These activities collectively support borneol’s therapeutic potential across multiple disease contexts.
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