Journal of Traditional Chinese Medicine ›› 2026, Vol. 46 ›› Issue (1): 39-50.DOI: 10.19852/j.cnki.jtcm.20250924.001
• Original Articles • Previous Articles Next Articles
Comparison of the effects of natural, cultivated, and synthetic musk on preventing acute cerebral ischemia/reperfusion injury in rats
LIANG Tianyu1, LIU Weiying2, TANG Huayang2, PENG Fu3, PENG Cheng1(
), PAN Xiaoqi2()
- 1 Cheng, Chinese Medicine Germplasm Resources Innovation and Effective Uses Key Laboratory of Sichuan Province, Chengdu University of Traditional Chinese Medicine, Chengdu 611130, China
2 School of Public Health, Chengdu University of Traditional Chinese Medicine, Chengdu 611130, China
3 West China School of Pharmacy, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu 610064, China
-
Received:2025-01-19Accepted:2025-05-20Online:2026-02-15Published:2025-09-24 -
Supported by:Key Project of National Natural Science Foundation of Sichuan: Research on the Mechanism of Detoxification and Synergistic Effects of Sichuan-Produced Toxic Authentic Medicinal Herbs Croton Seed and Aconite Root(2024NSFSC0054);National Interdisciplinary Innovation Team of Traditional Chinese Medicine:Multidisciplinary Innovation Team for Multidimensional Evaluation of Southwest Chinese Characteristic Traditional Chinese Medicine Resources(ZYYCXTD-D-202209);Sichuan Chinese Medicine Science and Technology Industry Innovation Team: Innovative Team for Multidimensional Evaluation and Product Development of Characteristic Traditional Chinese Medicine Resources(2022C001)
Cite this article
LIANG Tianyu, LIU Weiying, TANG Huayang, PENG Fu, PENG Cheng, PAN Xiaoqi. Comparison of the effects of natural, cultivated, and synthetic musk on preventing acute cerebral ischemia/reperfusion injury in rats[J]. Journal of Traditional Chinese Medicine, 2026, 46(1): 39-50.
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Figure 1 Musk prevents against acute CI/RI via ameliorating cerebral ischemia in rats A: images of TTC staining; B: statistical analysis of cerebral infarct area; C: HE staining of brain tissue sections (×200); D: the HE scores of rats after musk pretreatment; A1, C1: sham group; A2, C2: model group; A3, C3: aspirin group; A4, C4: natural group; A5, C5: cultivated group; A6, C6: synthetic group. Sham group: rats underwent the identical surgical procedure except that the proximal bifurcation of the common carotid artery was not ligated; model group: ligation of the proximal bifurcation of the common carotid artery in rats; aspirin group: model formation was performed 3 d after administration of 89 mg·kg?1·d?1 aspirin; natural group: model formation was performed 3 d after administration of 60 mg·kg?1·d?1 natural musk; cultivated group: model formation was performed 3 d after administration of 30 mg·kg?1·d?1 cultivated musk; synthetic group: model formation was performed 3 d after administration of 60 mg·kg?1·d?1 synthetic musk. CI/RI: acute cerebral ischemia/reperfusion injury; TTC: triphenyltetrazolium chloride; HE: hematoxylin-eosin staining. Differences in means between groups were examined using one-way analysis of variance, with the Dunnett’s T3 test used for the data in this table. Data were presented as mean ± standard error of the mean (n = 6). Significant differences compared with sham group were designated as aP < 0.05 and with sham group as bP < 0.01.
Figure 1 Musk prevents against acute CI/RI via ameliorating cerebral ischemia in rats A: images of TTC staining; B: statistical analysis of cerebral infarct area; C: HE staining of brain tissue sections (×200); D: the HE scores of rats after musk pretreatment; A1, C1: sham group; A2, C2: model group; A3, C3: aspirin group; A4, C4: natural group; A5, C5: cultivated group; A6, C6: synthetic group. Sham group: rats underwent the identical surgical procedure except that the proximal bifurcation of the common carotid artery was not ligated; model group: ligation of the proximal bifurcation of the common carotid artery in rats; aspirin group: model formation was performed 3 d after administration of 89 mg·kg?1·d?1 aspirin; natural group: model formation was performed 3 d after administration of 60 mg·kg?1·d?1 natural musk; cultivated group: model formation was performed 3 d after administration of 30 mg·kg?1·d?1 cultivated musk; synthetic group: model formation was performed 3 d after administration of 60 mg·kg?1·d?1 synthetic musk. CI/RI: acute cerebral ischemia/reperfusion injury; TTC: triphenyltetrazolium chloride; HE: hematoxylin-eosin staining. Differences in means between groups were examined using one-way analysis of variance, with the Dunnett’s T3 test used for the data in this table. Data were presented as mean ± standard error of the mean (n = 6). Significant differences compared with sham group were designated as aP < 0.05 and with sham group as bP < 0.01.
Figure 2 Musk prevents neuronal injury in MCAO/R rats A: Nissl staining; B: Nissl bodies count statistics of ischemic brain tissue sections; C: immunohistochemistry of ischemic NEUN protein content (×400); D: positive area proportion; A1, C1: sham group; A2, C2: model group; A3, C3: aspirin group; A4, C4: natural group; A5, C5: cultivated group; A6, C6: synthetic group. Sham group: rats underwent the identical surgical procedure except that the proximal bifurcation of the common carotid artery was not ligated; model group: ligation of the proximal bifurcation of the common carotid artery in rats; aspirin group: model formation was performed 3 d after administration of 89 mg·kg?1·d?1 aspirin; natural group: model formation was performed 3 days after administration of 60 mg·kg?1·d?1 natural musk; cultivated group: model formation was performed 3 d after administration of 30 mg·kg?1·d?1 cultivated musk; synthetic group: model formation was performed 3 d after administration of 60 mg·kg?1·d?1 synthetic musk. MCAO/R: middle cerebral artery occlusion reperfusion; NEUN: neuron-specific nuclear protein. Differences in means between groups were examined using one-way analysis of variance, with the Dunnett’s T3 test used for the data in this table. Data were presented as mean ± standard error of the mean (n = 6). Significant differences compared with sham group were designated as aP < 0.05 and with sham group as bP < 0.01.
Figure 2 Musk prevents neuronal injury in MCAO/R rats A: Nissl staining; B: Nissl bodies count statistics of ischemic brain tissue sections; C: immunohistochemistry of ischemic NEUN protein content (×400); D: positive area proportion; A1, C1: sham group; A2, C2: model group; A3, C3: aspirin group; A4, C4: natural group; A5, C5: cultivated group; A6, C6: synthetic group. Sham group: rats underwent the identical surgical procedure except that the proximal bifurcation of the common carotid artery was not ligated; model group: ligation of the proximal bifurcation of the common carotid artery in rats; aspirin group: model formation was performed 3 d after administration of 89 mg·kg?1·d?1 aspirin; natural group: model formation was performed 3 days after administration of 60 mg·kg?1·d?1 natural musk; cultivated group: model formation was performed 3 d after administration of 30 mg·kg?1·d?1 cultivated musk; synthetic group: model formation was performed 3 d after administration of 60 mg·kg?1·d?1 synthetic musk. MCAO/R: middle cerebral artery occlusion reperfusion; NEUN: neuron-specific nuclear protein. Differences in means between groups were examined using one-way analysis of variance, with the Dunnett’s T3 test used for the data in this table. Data were presented as mean ± standard error of the mean (n = 6). Significant differences compared with sham group were designated as aP < 0.05 and with sham group as bP < 0.01.
Figure 3 Musk prevents thrombosis in rats with acute CI/RI A1: electrophoresis band pattern; A2: the protein expression level of P2Y12 was measured by Western blotting; A3: the protein expression level of PAFR was measured by Western blotting; B: maximum platelet aggregation rate; C: levels of ADP were measured by ELISA; D: levels of PAF were measured by ELISA; E: levels of ET-1 were measured by ELISA; F: levels of TXA2 were measured by ELISA; G: levels of TXB2 were measured by ELISA. 1: sham group; 2: model group; 3: aspirin group; 4: natural group; 5: cultivated group; 6: synthetic group. Sham group: rats underwent the identical surgical procedure except that the proximal bifurcation of the common carotid artery was not ligated; model group: ligation of the proximal bifurcation of the common carotid artery in rats; aspirin group: model formation was performed 3 d after administration of 89 mg·kg?1·d?1 aspirin; natural group: model formation was performed 3 d after administration of 60 mg·kg?1·d?1 natural musk; cultivated group: model formation was performed 3 d after administration of 30 mg·kg?1·d?1 cultivated musk; synthetic group: model formation was performed 3 d after administration of 60 mg·kg?1·d?1 synthetic musk. P2Y12: anti-purinergic receptor; PAFR: platelet activating factor receptor; ADP: adenosine diphosphate; PAF: platelet-activating factor; ET-1: endothelin-1; TXA2: thromboxane A2; TXB2: thromboxane B2; CI/RI: cerebral ischemia/reperfusion injury; ELISA: enzyme-linked immunosorbent assay. Differences in means between groups were examined using one-way analysis of variance, with the Dunnett’s T3 test used for the data in this table. Data were presented as mean ± standard error of the mean (n = 6). Significant differences compared with sham group were designated as aP < 0.05 and with sham group as bP < 0.01.
Figure 3 Musk prevents thrombosis in rats with acute CI/RI A1: electrophoresis band pattern; A2: the protein expression level of P2Y12 was measured by Western blotting; A3: the protein expression level of PAFR was measured by Western blotting; B: maximum platelet aggregation rate; C: levels of ADP were measured by ELISA; D: levels of PAF were measured by ELISA; E: levels of ET-1 were measured by ELISA; F: levels of TXA2 were measured by ELISA; G: levels of TXB2 were measured by ELISA. 1: sham group; 2: model group; 3: aspirin group; 4: natural group; 5: cultivated group; 6: synthetic group. Sham group: rats underwent the identical surgical procedure except that the proximal bifurcation of the common carotid artery was not ligated; model group: ligation of the proximal bifurcation of the common carotid artery in rats; aspirin group: model formation was performed 3 d after administration of 89 mg·kg?1·d?1 aspirin; natural group: model formation was performed 3 d after administration of 60 mg·kg?1·d?1 natural musk; cultivated group: model formation was performed 3 d after administration of 30 mg·kg?1·d?1 cultivated musk; synthetic group: model formation was performed 3 d after administration of 60 mg·kg?1·d?1 synthetic musk. P2Y12: anti-purinergic receptor; PAFR: platelet activating factor receptor; ADP: adenosine diphosphate; PAF: platelet-activating factor; ET-1: endothelin-1; TXA2: thromboxane A2; TXB2: thromboxane B2; CI/RI: cerebral ischemia/reperfusion injury; ELISA: enzyme-linked immunosorbent assay. Differences in means between groups were examined using one-way analysis of variance, with the Dunnett’s T3 test used for the data in this table. Data were presented as mean ± standard error of the mean (n = 6). Significant differences compared with sham group were designated as aP < 0.05 and with sham group as bP < 0.01.
Table 1 Pretreatment with musk reduces the release of neurotransmitters in MCAO/R model rats
| Group | n | 5-HT content (ng/L) | Ach content (pmol/L) | AchE content (nmol/L) |
|---|---|---|---|---|
| Sham | 6 | 130±36 | 137±17 | 143±36 |
| Model | 6 | 216±44a | 173±23a | 248±56a |
| Aspirin | 6 | 134±39b | 135±26b | 162±20b |
| Natural | 6 | 195±32 | 140±12d | 181±33d |
| Cultivated | 6 | 141±40bc | 152±25 | 216±48 |
| Synthetic | 6 | 139±23b | 159±20 | 176±15b |
Table 1 Pretreatment with musk reduces the release of neurotransmitters in MCAO/R model rats
| Group | n | 5-HT content (ng/L) | Ach content (pmol/L) | AchE content (nmol/L) |
|---|---|---|---|---|
| Sham | 6 | 130±36 | 137±17 | 143±36 |
| Model | 6 | 216±44a | 173±23a | 248±56a |
| Aspirin | 6 | 134±39b | 135±26b | 162±20b |
| Natural | 6 | 195±32 | 140±12d | 181±33d |
| Cultivated | 6 | 141±40bc | 152±25 | 216±48 |
| Synthetic | 6 | 139±23b | 159±20 | 176±15b |
Table 2 Pre-administration of musk inhibits inflammation in MCAO/R model rats
| Group | n | TNF-α content (ng/L) | IL-1β content (ng/L) | IL-6 content (pg/mL) |
|---|---|---|---|---|
| Sham | 6 | 178.2±29.2 | 16.3±4.3 | 36.3±8.3 |
| Model | 6 | 257.1±15.2a | 24.8±4.0a | 61.4±11.4a |
| Aspirin | 6 | 193.2±23.0b | 17.7±3.8b | 35.1±7.8b |
| Natural | 6 | 233.5±8.1 | 23.1±2.8 | 34.9±7.6b |
| Cultivated | 6 | 225.6±34.5c | 19.5±5.4c | 48.4±6.7c |
| Synthetic | 6 | 209.6±19.6b | 19.9±2.9c | 58.7±13.9 |
Table 2 Pre-administration of musk inhibits inflammation in MCAO/R model rats
| Group | n | TNF-α content (ng/L) | IL-1β content (ng/L) | IL-6 content (pg/mL) |
|---|---|---|---|---|
| Sham | 6 | 178.2±29.2 | 16.3±4.3 | 36.3±8.3 |
| Model | 6 | 257.1±15.2a | 24.8±4.0a | 61.4±11.4a |
| Aspirin | 6 | 193.2±23.0b | 17.7±3.8b | 35.1±7.8b |
| Natural | 6 | 233.5±8.1 | 23.1±2.8 | 34.9±7.6b |
| Cultivated | 6 | 225.6±34.5c | 19.5±5.4c | 48.4±6.7c |
| Synthetic | 6 | 209.6±19.6b | 19.9±2.9c | 58.7±13.9 |
Table 3 Musk pretreatment enhances antioxidative ability in rats with acute CI/RI
| Group | n | CAT activity (U/mL) | SOD activity (U/mL) | NO content (μmol/mL) | iNOS activity (μmol/L) |
|---|---|---|---|---|---|
| Sham | 6 | 137.026±10.899 | 31.436±4.429 | 0.018±0.003 | 6.086±0.357 |
| Model | 6 | 99.918±16.672a | 19.176±3.392a | 0.074±0.040a | 7.257±0.785a |
| Aspirin | 6 | 135.953±16.265b | 24.064±2.246d | 0.023±0.007b | 6.616±0.267 |
| Natural | 6 | 94.711±26.555 | 27.568±6.394b | 0.031±0.030b | 6.327±0.885d |
| Cultivated | 6 | 125.155±14.091bc | 21.861±2.199c | 0.038±0.031d | 6.061±0.332be |
| Synthetic | 6 | 124.884±11.210b | 22.300±6.391 | 0.051±0.031 | 7.551±0.779 |
Table 3 Musk pretreatment enhances antioxidative ability in rats with acute CI/RI
| Group | n | CAT activity (U/mL) | SOD activity (U/mL) | NO content (μmol/mL) | iNOS activity (μmol/L) |
|---|---|---|---|---|---|
| Sham | 6 | 137.026±10.899 | 31.436±4.429 | 0.018±0.003 | 6.086±0.357 |
| Model | 6 | 99.918±16.672a | 19.176±3.392a | 0.074±0.040a | 7.257±0.785a |
| Aspirin | 6 | 135.953±16.265b | 24.064±2.246d | 0.023±0.007b | 6.616±0.267 |
| Natural | 6 | 94.711±26.555 | 27.568±6.394b | 0.031±0.030b | 6.327±0.885d |
| Cultivated | 6 | 125.155±14.091bc | 21.861±2.199c | 0.038±0.031d | 6.061±0.332be |
| Synthetic | 6 | 124.884±11.210b | 22.300±6.391 | 0.051±0.031 | 7.551±0.779 |
Figure 4 Musk enhances blood circulation of brains in rats A: laser speckle images of brain tissue at different time points following norepinephrine titration; A1: 0 min; A2: 5 min; A3: 10 min; A4: 15 min; A5: 20 min; A6: 25 min; A7: 30 min; A8: 0 min grayscale image; A9: 5 min grayscale image; A10: 10 min grayscale image; A11: 15 min grayscale image; A12: 20 min grayscale image; A13: 25 min grayscale image; A14: 30 min grayscale image; B: cerebral blood flow perfusion values at different time points; C: laser speckle images of brain tissue at 30 min after drug treatment; C1: control group; C2: norepinephrine; C3: natural group; C4: cultivated group; C5: synthetic group; C6: control group grayscale image; C7: norepinephrine group grayscale image; C8: natural group grayscale image; C9: cultivated group grayscale image; C10: synthetic group grayscale image; D: cerebral blood flow perfusion statistics 30 min after drug administration. Control group: 10 μL physiological saline solution; norepinephrine: 10 μL of 0.1% norepinephrine; natural group: 10 μL of natural musk; cultivated group: 10 μL of cultivated musk; synthetic group: 10 μL of synthetic musk. Differences in means between groups were examined using one-way analysis of variance, with the Dunnett’s T3 test used for the data in this table. Data were presented as mean ± standard error of the mean (n = 10). Significant differences compared with sham group were designated as aP < 0.05 and with sham group as bP < 0.01.
Figure 4 Musk enhances blood circulation of brains in rats A: laser speckle images of brain tissue at different time points following norepinephrine titration; A1: 0 min; A2: 5 min; A3: 10 min; A4: 15 min; A5: 20 min; A6: 25 min; A7: 30 min; A8: 0 min grayscale image; A9: 5 min grayscale image; A10: 10 min grayscale image; A11: 15 min grayscale image; A12: 20 min grayscale image; A13: 25 min grayscale image; A14: 30 min grayscale image; B: cerebral blood flow perfusion values at different time points; C: laser speckle images of brain tissue at 30 min after drug treatment; C1: control group; C2: norepinephrine; C3: natural group; C4: cultivated group; C5: synthetic group; C6: control group grayscale image; C7: norepinephrine group grayscale image; C8: natural group grayscale image; C9: cultivated group grayscale image; C10: synthetic group grayscale image; D: cerebral blood flow perfusion statistics 30 min after drug administration. Control group: 10 μL physiological saline solution; norepinephrine: 10 μL of 0.1% norepinephrine; natural group: 10 μL of natural musk; cultivated group: 10 μL of cultivated musk; synthetic group: 10 μL of synthetic musk. Differences in means between groups were examined using one-way analysis of variance, with the Dunnett’s T3 test used for the data in this table. Data were presented as mean ± standard error of the mean (n = 10). Significant differences compared with sham group were designated as aP < 0.05 and with sham group as bP < 0.01.
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